+ |
KAT6A/KAT6B | up-regulates
acetylation
|
TP53 |
0.492 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-217194 |
Lys120 |
FLHSGTAkSVTCTYS |
Homo sapiens |
Leukemia Cell |
pmid |
sentence |
23431171 |
We show here that moz is an acetyltransferase of p53 at k120 and k382 and colocalizes with p53 in promyelocytic leukemia (pml) nuclear bodies following cellular stress. The moz-pml-p53 interaction enhances moz-mediated acetylation of p53, and this ternary complex enhances p53-dependent p21 expression |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-217198 |
Lys382 |
QSTSRHKkLMFKTEG |
Homo sapiens |
Leukemia Cell |
pmid |
sentence |
23431171 |
We show here that moz is an acetyltransferase of p53 at k120 and k382 and colocalizes with p53 in promyelocytic leukemia (pml) nuclear bodies following cellular stress. The moz-pml-p53 interaction enhances moz-mediated acetylation of p53, and this ternary complex enhances p53-dependent p21 expression |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
NAT10 | up-regulates quantity by stabilization
acetylation
|
TP53 |
0.343 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-272406 |
Lys120 |
FLHSGTAkSVTCTYS |
Homo sapiens |
NCI-H1299 Cell |
pmid |
sentence |
26882543 |
NAT10 acetylates p53 at K120 and stabilizes p53 by counteracting Mdm2 action. In addition, NAT10 promotes Mdm2 degradation with its intrinsic E3 ligase activity. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
KAT6A | up-regulates
acetylation
|
TP53 |
0.656 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-201482 |
Lys120 |
FLHSGTAkSVTCTYS |
Homo sapiens |
Leukemia Cell |
pmid |
sentence |
23431171 |
We show here that moz is an acetyltransferase of p53 at k120 and k382 and colocalizes with p53 in promyelocytic leukemia (pml) nuclear bodies following cellular stress. The moz-pml-p53 interaction enhances moz-mediated acetylation of p53, and this ternary complex enhances p53-dependent p21 expression |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-201486 |
Lys382 |
QSTSRHKkLMFKTEG |
Homo sapiens |
Leukemia Cell |
pmid |
sentence |
23431171 |
We show here that moz is an acetyltransferase of p53 at k120 and k382 and colocalizes with p53 in promyelocytic leukemia (pml) nuclear bodies following cellular stress. The moz-pml-p53 interaction enhances moz-mediated acetylation of p53, and this ternary complex enhances p53-dependent p21 expression |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
MKRN1 | down-regulates quantity by destabilization
polyubiquitination
|
TP53 |
0.442 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-271846 |
Lys291 |
TEEENLRkKGEPHHE |
Homo sapiens |
NCI-H1299 Cell |
pmid |
sentence |
19536131 |
Makorin Ring Finger Protein 1 (MKRN1) is a transcriptional co-regulator and an E3 ligase. Here, we show that MKRN1 simultaneously functions as a differentially negative regulator of p53 and p21. In normal conditions, MKRN1 could destabilize both p53 and p21 through ubiquitination and proteasome-dependent degradation. As a result, depletion of MKRN1 induced growth arrest through activation of p53 and p21. K291 and K292 of p53 are required for MKRN1-mediated degradation and ubiquitination of p53 |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-271847 |
Lys292 |
EEENLRKkGEPHHEL |
Homo sapiens |
NCI-H1299 Cell |
pmid |
sentence |
19536131 |
Makorin Ring Finger Protein 1 (MKRN1) is a transcriptional co-regulator and an E3 ligase. Here, we show that MKRN1 simultaneously functions as a differentially negative regulator of p53 and p21. In normal conditions, MKRN1 could destabilize both p53 and p21 through ubiquitination and proteasome-dependent degradation. As a result, depletion of MKRN1 induced growth arrest through activation of p53 and p21. K291 and K292 of p53 are required for MKRN1-mediated degradation and ubiquitination of p53 |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
E4F1 | up-regulates activity
ubiquitination
|
TP53 |
0.591 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-271394 |
Lys319 |
TSSSPQPkKKPLDGE |
Homo sapiens |
U2-OS Cell |
pmid |
sentence |
17110336 |
E4F1 Has an Intrinsic Ubiquitin E3 Ligase Activity that Drives K48-type Ubiquitylation of p53. These data demonstrate that E4F1 stimulates the ubiquitylation of p53 on the lysine cluster K319–K321, i.e., at sites distinct from those targeted by Hdm2. p53 forms Ubiquitylated by E4F1 Are Localized on Chromatin. In striking contrast with Ub-p53 forms stimulated by Hdm2, which are mainly cytosoluble and targeted to the proteasome, we found that E4F1-stimulated Ub-p53 forms are tightly associated with chromatin, suggesting that they could be involved in transcription. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-271395 |
Lys321 |
SSPQPKKkPLDGEYF |
Homo sapiens |
U2-OS Cell |
pmid |
sentence |
17110336 |
E4F1 Has an Intrinsic Ubiquitin E3 Ligase Activity that Drives K48-type Ubiquitylation of p53. These data demonstrate that E4F1 stimulates the ubiquitylation of p53 on the lysine cluster K319–K321, i.e., at sites distinct from those targeted by Hdm2. p53 forms Ubiquitylated by E4F1 Are Localized on Chromatin. In striking contrast with Ub-p53 forms stimulated by Hdm2, which are mainly cytosoluble and targeted to the proteasome, we found that E4F1-stimulated Ub-p53 forms are tightly associated with chromatin, suggesting that they could be involved in transcription. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
FBXO11 | down-regulates
neddylation
|
TP53 |
0.657 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-150669 |
Lys320 |
SSSPQPKkKPLDGEY |
Homo sapiens |
|
pmid |
sentence |
17098746 |
Fbxo11 promotes the neddylation of p53 and inhibits its transcriptional activity / we found that fbxo11 also neddylates p53 on two lysines, lys-320 and lys-321 |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-150673 |
Lys321 |
SSPQPKKkPLDGEYF |
Homo sapiens |
|
pmid |
sentence |
17098746 |
Fbxo11 promotes the neddylation of p53 and inhibits its transcriptional activity / we found that fbxo11 also neddylates p53 on two lysines, lys-320 and lys-321 |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
EP300 | up-regulates
acetylation
|
TP53 |
0.909 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-84070 |
Lys373 |
SSHLKSKkGQSTSRH |
Homo sapiens |
HeLa Cell |
pmid |
sentence |
11070080 |
P300 acetylates and activates the tumor suppressor p53 after dna damage. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-84074 |
Lys382 |
QSTSRHKkLMFKTEG |
Homo sapiens |
HeLa Cell |
pmid |
sentence |
11070080 |
P300 acetylates and activates the tumor suppressor p53 after dna damage. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, p53 in cancer |
+ |
SIRT1 | down-regulates
deacetylation
|
TP53 |
0.796 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-182515 |
Lys382 |
QSTSRHKkLMFKTEG |
Homo sapiens |
Breast Cancer Cell |
pmid |
sentence |
19047049 |
Sirt1 has been shown to regulate cell fate in part by deacetylating the p53 protein at lysine 382 and inhibiting p53-mediated transcriptional activation and apoptosis. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML |
+ |
AURKA | up-regulates
phosphorylation
|
TP53 |
0.77 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-199939 |
Ser106 |
SQKTYQGsYGFRLGF |
Homo sapiens |
|
pmid |
sentence |
23201157 |
Ser-106 phosphorylation of p53 decreases its interaction with mdm2 and prolongs the half-life of p53 |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
ATM | up-regulates quantity by stabilization
phosphorylation
|
TP53 |
0.838 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-158632 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
|
pmid |
sentence |
17967874 |
In this study, we show that the increased interaction between B56gamma and p53 after DNA damage requires ATM-dependent phosphorylation of p53 at Ser15. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-167152 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
|
pmid |
sentence |
20663147 |
Deltanp63 transcriptionally regulates atm to control p53 serine-15 phosphorylation. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-126753 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
HaCaT Cell |
pmid |
sentence |
15254178 |
Deltanp63 transcriptionally regulates atm to control p53 serine-15 phosphorylation. We next aimed to identify novel factors that control damage-induced p53 phosphorylation in a keratinocyte model system, and discovered that the epithelial stem cell marker _Np63_ is a novel ATM regulator that controls p53 Serine-15 phosphorylation through transcription of the ATM kinase. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-115340 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
|
pmid |
sentence |
11875057 |
In response to ionizing radiation (ir), atm, the gene product mutated in ataxia telangiectasia, stabilizes and activates p53 through phosphorylation of ser15 and (indirectly) ser20. Here we show that phosphorylation of p53 on ser46, a residue important for p53 apoptotic activity, as well as on ser9, in response to ir also is dependent on the atm protein kinase. one pathway involves the phosphorylation of p53 and its negative regulator mdm2 by ataxia telangiectasia mutated (atm) and chk2 causing p53 activation and stabilization. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-158636 |
Ser20 |
PLSQETFsDLWKLLP |
Homo sapiens |
NCI-H1299 Cell |
pmid |
sentence |
17967874 |
The increased interaction between B56gamma and p53 after DNA damage requires ATM-dependent phosphorylation of p53 at Ser15. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-167156 |
Ser20 |
PLSQETFsDLWKLLP |
Homo sapiens |
HaCaT Cell |
pmid |
sentence |
20663147 |
DeltaNp63alpha depletion by RNAi reduces steady-state ATM mRNA and protein levels, and attenuates p53 Serine-15 phosphorylation. Conversely, ectopic expression of DeltaNp63alpha in p63-null tumour cells stimulates ATM transcription and p53 Serine-15 phosphorylation |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-126757 |
Ser20 |
PLSQETFsDLWKLLP |
Homo sapiens |
U2-OS Cell |
pmid |
sentence |
15254178 |
Although the stabilization of p53 was apparently concordant with its phosphorylation on N-terminal serine residues in HFFF-2 cells, it did not require the phosphorylation of Ser15 or Ser20 by ATM, a cellular kinase known to phosphorylate and promote the stabilization of p53 in response to DNA damage. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-115344 |
Ser46 |
AMDDLMLsPDDIEQW |
Homo sapiens |
|
pmid |
sentence |
11875057 |
In response to ionizing radiation (ir), atm, the gene product mutated in ataxia telangiectasia, stabilizes and activates p53 through phosphorylation of ser15 and (indirectly) ser20. Here we show that phosphorylation of p53 on ser46, a residue important for p53 apoptotic activity, as well as on ser9, in response to ir also is dependent on the atm protein kinase. one pathway involves the phosphorylation of p53 and its negative regulator mdm2 by ataxia telangiectasia mutated (atm) and chk2 causing p53 activation and stabilization. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-115348 |
Ser9 |
EEPQSDPsVEPPLSQ |
Homo sapiens |
|
pmid |
sentence |
11875057 |
In response to ionizing radiation (ir), atm, the gene product mutated in ataxia telangiectasia, stabilizes and activates p53 through phosphorylation of ser15 and (indirectly) ser20. Here we show that phosphorylation of p53 on ser46, a residue important for p53 apoptotic activity, as well as on ser9, in response to ir also is dependent on the atm protein kinase. one pathway involves the phosphorylation of p53 and its negative regulator mdm2 by ataxia telangiectasia mutated (atm) and chk2 causing p53 activation and stabilization. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-151138 |
|
|
Homo sapiens |
|
pmid |
sentence |
17157788 |
Atm/atr are generally sensors of dna damage, but, together with the checkpoint kinases chk1 and chk2, they also function as response effectors by phosphorylation of key substrates, such as p53, brca1, and nbs1. In particular, p53 phosphorylation leads to protein accumulation and activation, which in turn promotes cell-cycle arrest or apoptosis. |
|
Publications: |
10 |
Organism: |
Homo Sapiens |
Pathways: | Colorectal Carcinoma, FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer |
+ |
DYRK1A | up-regulates
phosphorylation
|
TP53 |
0.428 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-167407 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
Neuron |
pmid |
sentence |
20696760 |
Dyrk1a phosphorylates p53 and inhibits proliferation of embryonic neuronal cells. we found that dyrk1a phosphorylates p53 at ser-15 in vitro and in immortalized rat embryonic hippocampal progenitor h19-7 cells. In addition, dyrk1a-induced p53 phosphorylation at ser-15 led to a robust induction of p53 target genes |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
AMPK | up-regulates
phosphorylation
|
TP53 |
0.421 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-216475 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
|
pmid |
sentence |
15866171 |
Ampk activation induces phosphorylation of p53 on serine 15, and this phosphorylation is required to initiate ampk-dependent cell-cycle arrest |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, IDH-TET in AML, FLT3-ITD signaling, Glycolysis and Gluconeogenesis, NPM1_new |
+ |
PPP1CA | down-regulates activity
dephosphorylation
|
TP53 |
0.32 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-248556 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
|
pmid |
sentence |
16501611 |
Protein serine/threonine phosphatase-1 dephosphorylates p53 at Ser-15 and Ser-37 to modulate its transcriptional and apoptotic activities|In addition, our results reveal that one of the molecular mechanisms by which PP-1 promotes cell survival is to dephosphorylate p53, and thus negatively regulate p53-dependent death pathway. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-248557 |
Ser37 |
NVLSPLPsQAMDDLM |
Homo sapiens |
|
pmid |
sentence |
16501611 |
Protein serine/threonine phosphatase-1 dephosphorylates p53 at Ser-15 and Ser-37 to modulate its transcriptional and apoptotic activities|In addition, our results reveal that one of the molecular mechanisms by which PP-1 promotes cell survival is to dephosphorylate p53, and thus negatively regulate p53-dependent death pathway. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
ATR | up-regulates quantity by stabilization
phosphorylation
|
TP53 |
0.731 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-115134 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
|
pmid |
sentence |
11865061 |
Nhibition of atr kinase activity substantially reduces hypoxia-induced phosphorylation of p53 protein on serine 15 as well as p53 protein accumulation. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer |
+ |
SMG1 | up-regulates
phosphorylation
|
TP53 |
0.422 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-125135 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
|
pmid |
sentence |
15175154 |
Hsmg-1 is a stress-activated kinase that phosphorylates p53 and hupf1 in vitrothe observation that hsmg-1 exhibits p53 (ser-15) kinase activity in vitro suggested that this pikk might be involved in genotoxic stress-induced p53 phosphorylation and stabilization in intact cells. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CHEK2 | up-regulates quantity by stabilization
phosphorylation
|
TP53 |
0.784 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-75009 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
HeLa Cell |
pmid |
sentence |
10673501 |
Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-75629 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
|
pmid |
sentence |
10710310 |
Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-153463 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
|
pmid |
sentence |
17339337 |
Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability. We have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-74823 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
|
pmid |
sentence |
10656682 |
Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-77144 |
Ser20 |
PLSQETFsDLWKLLP |
Homo sapiens |
|
pmid |
sentence |
10801407 |
The tumour suppressor protein p53 is stabilised and activated in response to ionising radiation. This is known to depend on the kinase atm;recent results suggest atm acts via the downstream kinase chk2/hcds1, which stabilises p53 at least in part by direct phosphorylation of residue serine 20 |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-75013 |
Ser366 |
PGGSRAHsSHLKSKK |
Homo sapiens |
HeLa Cell |
pmid |
sentence |
10673501 |
Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-75633 |
Ser366 |
PGGSRAHsSHLKSKK |
Homo sapiens |
LNCaP Cell |
pmid |
sentence |
15659650 |
The cell cycle checkpoint kinases CHK1 and CHK2 have been shown to phosphorylate multiple sites in the N-terminal domain of p53, consequently leading to p53 stabilization and activation. Phosphorylation of at least three of these sites, Ser366, Ser378, and Thr387, was induced by DNA damage. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-75637 |
Ser37 |
NVLSPLPsQAMDDLM |
Homo sapiens |
|
pmid |
sentence |
10710310 |
Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-75017 |
Ser37 |
NVLSPLPsQAMDDLM |
Homo sapiens |
HeLa Cell |
pmid |
sentence |
10673501 |
Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-74831 |
Ser37 |
NVLSPLPsQAMDDLM |
Homo sapiens |
|
pmid |
sentence |
10656682 |
Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-153475 |
Ser37 |
NVLSPLPsQAMDDLM |
Homo sapiens |
|
pmid |
sentence |
15659650 |
The cell cycle checkpoint kinases CHK1 and CHK2 have been shown to phosphorylate multiple sites in the N-terminal domain of p53, consequently leading to p53 stabilization and activation. Phosphorylation of at least three of these sites, Ser366, Ser378, and Thr387, was induced by DNA damage. On activation, both of these kinases also phosphorylate multiple sites in the p53 N-terminal domain. These include Ser15, Thr18, Ser20, and Ser37, which are all DNA-damageinducible sites |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-153479 |
Ser378 |
SKKGQSTsRHKKLMF |
Homo sapiens |
B-lymphocyte |
pmid |
sentence |
17339337 |
Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-75641 |
Ser378 |
SKKGQSTsRHKKLMF |
Homo sapiens |
|
pmid |
sentence |
10710310 |
Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-74835 |
Ser378 |
SKKGQSTsRHKKLMF |
Homo sapiens |
LNCaP Cell |
pmid |
sentence |
15659650 |
The cell cycle checkpoint kinases CHK1 and CHK2 have been shown to phosphorylate multiple sites in the N-terminal domain of p53, consequently leading to p53 stabilization and activation. Phosphorylation of at least three of these sites, Ser366, Ser378, and Thr387, was induced by DNA damage. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-75025 |
Thr18 |
EPPLSQEtFSDLWKL |
Homo sapiens |
HeLa Cell |
pmid |
sentence |
10673501 |
Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-74839 |
Thr18 |
EPPLSQEtFSDLWKL |
Homo sapiens |
|
pmid |
sentence |
10656682 |
Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-153483 |
Thr18 |
EPPLSQEtFSDLWKL |
Homo sapiens |
B-lymphocyte |
pmid |
sentence |
17339337 |
Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-75645 |
Thr18 |
EPPLSQEtFSDLWKL |
Homo sapiens |
|
pmid |
sentence |
10710310 |
Chk1/chk2 and atm/atr also phosphorylate the effector p53, increasing its stability.We Have demonstrated that the human homologs of the checkpoint kinases, chk1 and chk2/hcds1, phosphorylate at least three dna damage-inducible phosphorylation sites in p53. |
|
Publications: |
18 |
Organism: |
Homo Sapiens |
Pathways: | FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer |
+ |
MAPK14 | up-regulates
phosphorylation
|
TP53 |
0.764 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-105737 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
MCF-7 Cell |
pmid |
sentence |
11258706 |
P38 regulates p53, but also in p53-defective tumor cells rewire their checkpoint response and become dependent in the p38/mk2 pathway in mcf-7 cells, p38 kinase activated p53 more effectively than other members of the ras pathway. p53 and p38 kinase exist in the same physical complex, and co-expression of p38 stabilized p53 protein. In vitro, p38 kinase phosphorylated p53 at ser33 and ser46, a newly identified site. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-105741 |
Ser33 |
LPENNVLsPLPSQAM |
Homo sapiens |
MCF-7 Cell |
pmid |
sentence |
11258706 |
P38 regulates p53, but also in p53-defective tumor cells rewire their checkpoint response and become dependent in the p38/mk2 pathway in mcf-7 cells, p38 kinase activated p53 more effectively than other members of the ras pathway. p53 and p38 kinase exist in the same physical complex, and co-expression of p38 stabilized p53 protein. In vitro, p38 kinase phosphorylated p53 at ser33 and ser46, a newly identified site. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-192057 |
Ser33 |
LPENNVLsPLPSQAM |
Homo sapiens |
MCF-7 Cell |
pmid |
sentence |
22975381 |
P38 regulates p53, but also in p53-defective tumor cells rewire their checkpoint response and become dependent in the p38/mk2 pathway in mcf-7 cells, p38 kinase activated p53 more effectively than other members of the ras pathway. p53 and p38 kinase exist in the same physical complex, and co-expression of p38 stabilized p53 protein. In vitro, p38 kinase phosphorylated p53 at ser33 and ser46, a newly identified site. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-155242 |
Ser33 |
LPENNVLsPLPSQAM |
Homo sapiens |
MCF-7 Cell |
pmid |
sentence |
17535811 |
P38 regulates p53, but also in p53-defective tumor cells rewire their checkpoint response and become dependent in the p38/mk2 pathway in mcf-7 cells, p38 kinase activated p53 more effectively than other members of the ras pathway. p53 and p38 kinase exist in the same physical complex, and co-expression of p38 stabilized p53 protein. In vitro, p38 kinase phosphorylated p53 at ser33 and ser46, a newly identified site. |
|
Publications: |
4 |
Organism: |
Homo Sapiens |
Pathways: | FLT3-ITD signaling, P38 Signaling |
+ |
CHEK1 | up-regulates activity
phosphorylation
|
TP53 |
0.772 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-217791 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
LNCaP Cell |
pmid |
sentence |
15659650 |
CHK1 and CHK2 phosphorylate the p53 N terminus at Ser15, Thr18, Ser20, and Ser37 |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-217795 |
Ser20 |
PLSQETFsDLWKLLP |
Homo sapiens |
LNCaP Cell |
pmid |
sentence |
15659650 |
CHK1 and CHK2 phosphorylate the p53 N terminus at Ser15, Thr18, Ser20, and Ser37 |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-217853 |
Ser366 |
PGGSRAHsSHLKSKK |
Homo sapiens |
LNCaP Cell |
pmid |
sentence |
15659650 |
Phosphorylation by chk1 of at least three of these sites, Ser366, Ser378, and Thr387, was induced by DNA damage. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-217799 |
Ser37 |
NVLSPLPsQAMDDLM |
Homo sapiens |
LNCaP Cell |
pmid |
sentence |
15659650 |
CHK1 and CHK2 phosphorylate the p53 N terminus at Ser15, Thr18, Ser20, and Ser37 |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-217857 |
Ser378 |
SKKGQSTsRHKKLMF |
Homo sapiens |
|
pmid |
sentence |
15659650 |
Phosphorylation by chk1 of at least three of these sites, Ser366, Ser378, and Thr387, was induced by DNA damage. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-217803 |
Thr18 |
EPPLSQEtFSDLWKL |
Homo sapiens |
|
pmid |
sentence |
15659650 |
CHK1 and CHK2 phosphorylate the p53 N terminus at Ser15, Thr18, Ser20, and Ser37 |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-217861 |
Thr387 |
HKKLMFKtEGPDSD |
Homo sapiens |
LNCaP Cell |
pmid |
sentence |
15659650 |
Phosphorylation by chk1 of at least three of these sites, Ser366, Ser378, and Thr387, was induced by DNA damage. |
|
Publications: |
7 |
Organism: |
Homo Sapiens |
Pathways: | FLT3-ITD signaling, Cell cycle: G2/M phase transition |
+ |
MAPK14 | up-regulates activity
phosphorylation
|
TP53 |
0.764 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-72695 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
MCF-7 Cell |
pmid |
sentence |
10581258 |
P38 regulates p53, but also in p53-defective tumor cells rewire their checkpoint response and become dependent in the p38/mk2 pathway in mcf-7 cells, p38 kinase activated p53 more effectively than other members of the ras pathway. p53 and p38 kinase exist in the same physical complex, and co-expression of p38 stabilized p53 protein. In vitro, p38 kinase phosphorylated p53 at ser33 and ser46, a newly identified site. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-72699 |
Ser33 |
LPENNVLsPLPSQAM |
Homo sapiens |
MCF-7 Cell |
pmid |
sentence |
10581258 |
P38 regulates p53, but also in p53-defective tumor cells rewire their checkpoint response and become dependent in the p38/mk2 pathway in mcf-7 cells, p38 kinase activated p53 more effectively than other members of the ras pathway. p53 and p38 kinase exist in the same physical complex, and co-expression of p38 stabilized p53 protein. In vitro, p38 kinase phosphorylated p53 at ser33 and ser46, a newly identified site. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-250114 |
Ser392 |
FKTEGPDsD |
|
|
pmid |
sentence |
10747897 |
We demonstrate that anisomycin- and tumor necrosis factor--induced phosphorylation of p53 at Ser-392, which is important for the transcriptional activity of this growth suppressor protein, requires p38 MAP kinase |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-72703 |
Ser46 |
AMDDLMLsPDDIEQW |
Homo sapiens |
MCF-7 Cell |
pmid |
sentence |
10581258 |
P38 regulates p53, but also in p53-defective tumor cells rewire their checkpoint response and become dependent in the p38/mk2 pathway in mcf-7 cells, p38 kinase activated p53 more effectively than other members of the ras pathway. p53 and p38 kinase exist in the same physical complex, and co-expression of p38 stabilized p53 protein. In vitro, p38 kinase phosphorylated p53 at ser33 and ser46, a newly identified site. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-155246 |
Ser46 |
AMDDLMLsPDDIEQW |
Homo sapiens |
MCF-7 Cell |
pmid |
sentence |
17535811 |
P38 regulates p53, but also in p53-defective tumor cells rewire their checkpoint response and become dependent in the p38/mk2 pathway in mcf-7 cells, p38 kinase activated p53 more effectively than other members of the ras pathway. p53 and p38 kinase exist in the same physical complex, and co-expression of p38 stabilized p53 protein. In vitro, p38 kinase phosphorylated p53 at ser33 and ser46, a newly identified site. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-226620 |
Ser46 |
AMDDLMLsPDDIEQW |
Homo sapiens |
HeLa Cell |
pmid |
sentence |
15642743 |
Recombinant p38 phosphorylated recombinant p53 on serine 46 in vitro. Inhibition of p38 MAPK by pharmacological inhibitors, dominant-negative p38, or small interfering RNA, suppressed p53S46P |
|
Publications: |
6 |
Organism: |
Homo Sapiens, |
Pathways: | FLT3-ITD signaling, P38 Signaling |
+ |
PRKDC | up-regulates
phosphorylation
|
TP53 |
0.785 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-53030 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
|
pmid |
sentence |
9363941 |
We demonstrate that phosphorylation of p53 at serines 15 and 37 impairs the ability of mdm2 to inhibit p53-dependent transactivation. We present evidence that these effects are most likely due to a conformational change induced upon phosphorylation of p53. Our studies provide a plausible mechanism by which the induction of p53 can be modulated by dna-pk (or other protein kinases with similar specificity) in response to dna damage. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Cell cycle: G2/M phase transition |
+ |
TP53RK | up-regulates
phosphorylation
|
TP53 |
0.751 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-157471 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
|
pmid |
sentence |
17712528 |
The intrinsic transcriptional activity of p53 was up-regulated by a transient transfection of prpk to cos-7 cells. Prpk was shown to bind to p53 and to phosphorylate p53 at ser-15. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
PPP1CC | down-regulates activity
dephosphorylation
|
TP53 |
0.323 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-248499 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
|
pmid |
sentence |
16501611 |
Protein serine/threonine phosphatase-1 dephosphorylates p53 at Ser-15 and Ser-37 to modulate its transcriptional and apoptotic activities|In addition, our results reveal that one of the molecular mechanisms by which PP-1 promotes cell survival is to dephosphorylate p53, and thus negatively regulate p53-dependent death pathway. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-248500 |
Ser37 |
NVLSPLPsQAMDDLM |
Homo sapiens |
|
pmid |
sentence |
16501611 |
Protein serine/threonine phosphatase-1 dephosphorylates p53 at Ser-15 and Ser-37 to modulate its transcriptional and apoptotic activities|In addition, our results reveal that one of the molecular mechanisms by which PP-1 promotes cell survival is to dephosphorylate p53, and thus negatively regulate p53-dependent death pathway. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
MAPK3 | up-regulates
phosphorylation
|
TP53 |
0.697 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-100270 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
|
pmid |
sentence |
12955074 |
Mutant p53 is constitutively phosphorylated at serine 15 in uv-induced mouse skin tumors: involvement of erk1/2 map kinase. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
PPM1D | down-regulates quantity by destabilization
dephosphorylation
|
TP53 |
0.576 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-276943 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
|
pmid |
sentence |
18265945 |
Dephosphorylation of p53 at serine 15 by Wip1 also contributes to p53 degradation, as does dephosphorylation of Mdm2, which stabilizes Mdm2, an E3 ubiquitin ligase specific for p53 [ xref ]. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | P38 Signaling |
+ |
NUAK1 | up-regulates
phosphorylation
|
TP53 |
0.527 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-172008 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
|
pmid |
sentence |
21317932 |
Here we showed that in the presence of wild-type lkb1, nuak1 directly interacts with and phosphorylates p53 in vitro and in vivo. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-172012 |
Ser392 |
FKTEGPDsD |
Homo sapiens |
|
pmid |
sentence |
21317932 |
Here we showed that in the presence of wild-type lkb1, nuak1 directly interacts with and phosphorylates p53 in vitro and in vivo. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
MAPK14 | up-regulates quantity by stabilization
phosphorylation
|
TP53 |
0.764 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-226614 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
JB6 Cl41 Cell |
pmid |
sentence |
10781582 |
Serine 15 phosphorylation of p53 leads to a stabilization of p53 by reducing its interaction with murine double minute 2, a negative regulatory partner[...]These results strongly suggest that both ERKs and p38 kinase have a direct role in UVB-induced phosphorylation of p53 at serine 15 in vivo. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | FLT3-ITD signaling, P38 Signaling |
+ |
PPM1D | down-regulates activity
dephosphorylation
|
TP53 |
0.576 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-248319 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
|
pmid |
sentence |
15870257 |
PPM1D binds Chk1 and dephosphorylates the ATR-targeted phospho-Ser 345, leading to decreased Chk1 kinase activity. PPM1D also dephosphorylates p53 at phospho-Ser 15. PPM1D dephosphorylations are correlated with reduced cellular intra-S and G2/M checkpoint activity in response to DNA damage induced by ultraviolet and ionizing radiation. Thus, a primary function of PPM1D may be to reverse the p53 and Chk1-induced DNA damage and cell cycle checkpoint responses and return the cell to a homeostatic state following completion of DNA repair. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | P38 Signaling |
+ |
PRKAA1 | up-regulates
phosphorylation
|
TP53 |
0.458 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-135960 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
|
pmid |
sentence |
15866171 |
Ampk activation induces phosphorylation of p53 on serine 15, and this phosphorylation is required to initiate ampk-dependent cell-cycle arrest |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CDK5 | up-regulates
phosphorylation
|
TP53 |
0.722 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-156414 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
Neuron |
pmid |
sentence |
17591690 |
Here, we demonstrate for the first time that cdk5 interacts with p53 and increases its stability through posttranslational regulation, leading to accumulation of p53, particularly in the nucleus. We show that cdk5 phosphorylates p53 on ser15, ser33 and ser46 in vitro, |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-156418 |
Ser20 |
PLSQETFsDLWKLLP |
Homo sapiens |
Neuron |
pmid |
sentence |
17591690 |
Here, we demonstrate for the first time that cdk5 interacts with p53 and increases its stability through posttranslational regulation, leading to accumulation of p53, particularly in the nucleus. We show that cdk5 phosphorylates p53 on ser15, ser33 and ser46 in vitro, |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-156422 |
Ser33 |
LPENNVLsPLPSQAM |
Homo sapiens |
|
pmid |
sentence |
17591690 |
We show that cdk5 phosphorylates p53 on ser15, ser33 and ser46 cdk5-stabilized p53 protein is transcriptionally active |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-156426 |
Ser46 |
AMDDLMLsPDDIEQW |
Homo sapiens |
Neuron |
pmid |
sentence |
17591690 |
We show that cdk5 phosphorylates p53 on ser15, ser33 and ser46 cdk5-stabilized p53 protein is transcriptionally active |
|
Publications: |
4 |
Organism: |
Homo Sapiens |
+ |
PP1 | down-regulates activity
dephosphorylation
|
TP53 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-264670 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
|
pmid |
sentence |
16501611 |
Protein serine/threonine phosphatase-1 dephosphorylates p53 at Ser-15 and Ser-37 to modulate its transcriptional and apoptotic activities|In addition, our results reveal that one of the molecular mechanisms by which PP-1 promotes cell survival is to dephosphorylate p53, and thus negatively regulate p53-dependent death pathway. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
PPM1D | down-regulates
dephosphorylation
|
TP53 |
0.576 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-135980 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
|
pmid |
sentence |
15870257 |
PPM1D also dephosphorylates p53 at phospho-Ser 15. PPM1D dephosphorylations are correlated with reduced cellular intra-S and G2/M checkpoint activity in response to DNA damage induced by ultraviolet and ionizing radiation. Thus, a primary function of PPM1D may be to reverse the p53 and Chk1-induced DNA damage and cell cycle checkpoint responses and return the cell to a homeostatic state following completion of DNA repair. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | P38 Signaling |
+ |
STK11 | up-regulates
phosphorylation
|
TP53 |
0.747 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-150830 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
|
pmid |
sentence |
17108107 |
We show that lkb1 physically associates with p53 in the nucleus and directly or indirectly phosphorylates p53 ser15 (previously shown to be phosphorylated by amp-dependent kinase) and p53 ser392 |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-150834 |
Ser392 |
FKTEGPDsD |
Homo sapiens |
|
pmid |
sentence |
17108107 |
We show that lkb1 physically associates with p53 in the nucleus and directly or indirectly phosphorylates p53 ser15 (previously shown to be phosphorylated by amp-dependent kinase) and p53 ser392 |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
Pathways: | FLT3-ITD signaling |
+ |
PPP1CB | down-regulates activity
dephosphorylation
|
TP53 |
0.29 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-248572 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
|
pmid |
sentence |
16501611 |
Protein serine/threonine phosphatase-1 dephosphorylates p53 at Ser-15 and Ser-37 to modulate its transcriptional and apoptotic activities|In addition, our results reveal that one of the molecular mechanisms by which PP-1 promotes cell survival is to dephosphorylate p53, and thus negatively regulate p53-dependent death pathway. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-248573 |
Ser37 |
NVLSPLPsQAMDDLM |
Homo sapiens |
|
pmid |
sentence |
16501611 |
Protein serine/threonine phosphatase-1 dephosphorylates p53 at Ser-15 and Ser-37 to modulate its transcriptional and apoptotic activities|In addition, our results reveal that one of the molecular mechanisms by which PP-1 promotes cell survival is to dephosphorylate p53, and thus negatively regulate p53-dependent death pathway. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
AURKB | down-regulates
phosphorylation
|
TP53 |
0.708 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-197598 |
Ser183 |
CPHHERCsDSDGLAP |
Homo sapiens |
|
pmid |
sentence |
22611192 |
We show that aurora b phosphorylates p53 at s183, t211, and s215 to accelerate the degradation of p53 through the polyubiquitination-proteasome pathway, thus functionally suppressing the expression of p53 target genes involved in cell cycle inhibition and apoptosis (e.g., p21 and puma). |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-197602 |
Ser215 |
DRNTFRHsVVVPYEP |
Homo sapiens |
|
pmid |
sentence |
22611192 |
We show that aurora b phosphorylates p53 at s183, t211, and s215 to accelerate the degradation of p53 through the polyubiquitination-proteasome pathway, thus functionally suppressing the expression of p53 target genes involved in cell cycle inhibition and apoptosis (e.g., p21 and puma). |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-168745 |
Ser269 |
GNLLGRNsFEVRVCA |
Homo sapiens |
|
pmid |
sentence |
20959462 |
Importantly, the aurora b-mediated phosphorylation on ser(269) or thr(284) significantly compromises p53 transcriptional activity. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-197606 |
Thr211 |
EYLDDRNtFRHSVVV |
Homo sapiens |
|
pmid |
sentence |
22611192 |
We show that aurora b phosphorylates p53 at s183, t211, and s215 to accelerate the degradation of p53 through the polyubiquitination-proteasome pathway, thus functionally suppressing the expression of p53 target genes involved in cell cycle inhibition and apoptosis (e.g., p21 and puma). |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-168749 |
Thr284 |
CPGRDRRtEEENLRK |
Homo sapiens |
|
pmid |
sentence |
20959462 |
Importantly, the aurora b-mediated phosphorylation on ser(269) or thr(284) significantly compromises p53 transcriptional activity. |
|
Publications: |
5 |
Organism: |
Homo Sapiens |
+ |
CSNK1A1 |
phosphorylation
|
TP53 |
0.58 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-162648 |
Ser20 |
PLSQETFsDLWKLLP |
Homo sapiens |
|
pmid |
sentence |
20041275 |
Our data support the concept that non-primed phosphorylation of p53 by ck1 is an isoform-specific reaction preferentially affecting s20 |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CHEK2 | up-regulates activity
phosphorylation
|
TP53 |
0.784 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-260776 |
Ser20 |
PLSQETFsDLWKLLP |
Homo sapiens |
|
pmid |
sentence |
17339337 |
Evaluation of these calcium calmodulin kinase superfamily members as candidate Ser(20) kinases in vivo has shown that only CHK1 or DAPK-1 can stimulate p53 transactivation and induce Ser(20) phosphorylation of p53.| Thus, endogenous CHK1 is required for the majority of Ser20 site phosphorylation of ectopically expressed p53 in H1299 cells. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer |
+ |
DAPK3 | up-regulates
phosphorylation
|
TP53 |
0.415 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-153495 |
Ser20 |
PLSQETFsDLWKLLP |
Homo sapiens |
B-lymphocyte |
pmid |
sentence |
17339337 |
A cell-free ser(20) phosphorylation site assay was used to identify a broad range of calcium calmodulin kinase superfamily members, including chk2, chk1, dapk-1, dapk-3, drak-1, and ampk, as ser(20) kinases.Evaluation of these calcium calmodulin kinase superfamily members as candidate ser(20) kinases in vivo has shown that only chk1 or dapk-1 can stimulate p53 transactivation and induce ser(20) phosphorylation of p53. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MAPK8 | up-regulates activity
phosphorylation
|
TP53 |
0.789 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-106538 |
Ser20 |
PLSQETFsDLWKLLP |
Mus musculus |
JB6 Cell |
pmid |
sentence |
11896587 |
Serine 20 phosphorylation of p53 has been shown to be required for the activation of p53 following UV radiation. we determined the role of map kinases in uvb-induced phosphorylation and found that jnks are directly involved in the phosphorylation of p53 at serine 20 |
|
Publications: |
1 |
Organism: |
Mus Musculus |
Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML |
+ |
MAPK9 | up-regulates
phosphorylation
|
TP53 |
0.738 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-115835 |
Ser20 |
PLSQETFsDLWKLLP |
Homo sapiens |
|
pmid |
sentence |
11896587 |
These findings strongly suggest that jnks are the major direct signaling mediators of uvb-induced p53 phosphorylation at serine 20. furthermore, phosphorylation of p53 at serine 20 by uvb-activated jnks and uvb-induced p53-dependent transcriptional activity were suppressed in jnk1 or jnk2 knockout (jnk1(-/-) or jnk2(-/-)) cells. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-155209 |
Ser6 |
sDPSVEPP |
Homo sapiens |
|
pmid |
sentence |
17525747 |
Our studies revealed a novel mechanism in which phosphorylation of jnk2 is mediated by jnk1 before phosphorylation of p53, and then p53 is directly phosphorylated by jnk2 at ser6. |Role of map kinases in uvb-induced phosphorylation of p53 at serine 20. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
CSNK1D | up-regulates
phosphorylation
|
TP53 |
0.559 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-75889 |
Ser20 |
PLSQETFsDLWKLLP |
Homo sapiens |
|
pmid |
sentence |
10734067 |
Here we show that the direct association between a p53 n-terminal peptide and mdm2 is disrupted by phosphorylation of the peptide on thr(18) but not by phosphorylation at other n-terminal sites, including ser(15) and ser(37). Thr(18) was phosphorylated in vitro by casein kinase (ck1). |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-73266 |
Ser20 |
PLSQETFsDLWKLLP |
Homo sapiens |
|
pmid |
sentence |
10606744 |
Protein kinase ck1 is a p53-threonine 18 kinase which requires prior phosphorylation of serine 15. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-73270 |
Thr18 |
EPPLSQEtFSDLWKL |
Homo sapiens |
|
pmid |
sentence |
10606744 |
Protein kinase ck1 is a p53-threonine 18 kinase which requires prior phosphorylation of serine 15. |
|
Publications: |
3 |
Organism: |
Homo Sapiens |
+ |
DUSP26 | down-regulates activity
dephosphorylation
|
TP53 |
0.374 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-248765 |
Ser20 |
PLSQETFsDLWKLLP |
Homo sapiens |
|
pmid |
sentence |
20562916 |
Dual-specificity phosphatase 26 is a novel p53 phosphatase and inhibits p53 tumor suppressor functions in human neuroblastoma|Inhibiting DUSP26 expression in the IMR-32 neuroblastoma cell line enhanced doxorubicin-induced p53 phosphorylation at Ser20 and Ser37, p21, Puma, Bax expression as well as apoptosis |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-248766 |
Ser37 |
NVLSPLPsQAMDDLM |
Homo sapiens |
|
pmid |
sentence |
20562916 |
Dual-specificity phosphatase 26 is a novel p53 phosphatase and inhibits p53 tumor suppressor functions in human neuroblastoma|Inhibiting DUSP26 expression in the IMR-32 neuroblastoma cell line enhanced doxorubicin-induced p53 phosphorylation at Ser20 and Ser37, p21, Puma, Bax expression as well as apoptosis |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
PLK3 | up-regulates activity
phosphorylation
|
TP53 |
0.694 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-109239 |
Ser20 |
PLSQETFsDLWKLLP |
Homo sapiens |
Fibroblast |
pmid |
sentence |
11447225 |
Upon exposure of cells to hydrogen peroxide (h(2)o(2)) phosphorylation of p53 was rapidly induced in human fibroblast gm00637, and this phosphorylation occurred on serine 9, serine 15, serine 20, but not on serine 392. In addition, h(2)o(2)-induced phosphorylation of p53 was followed by induction of p21, suggesting functional activation of p53. Ectopic expression of a plk3 dominant negative mutant, plk3(k52r), in gm00637 cells suppressed h(2)o(2)-induced serine 20 phosphorylation. Taken together, our studies strongly suggest that the oxidative stress-induced activation of p53 is at least in part mediated by plk3. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MAPK8 | up-regulates
phosphorylation
|
TP53 |
0.789 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-115831 |
Ser20 |
PLSQETFsDLWKLLP |
Homo sapiens |
|
pmid |
sentence |
11896587 |
These findings strongly suggest that jnks are the major direct signaling mediators of uvb-induced p53 phosphorylation at serine 20. furthermore, phosphorylation of p53 at serine 20 by uvb-activated jnks and uvb-induced p53-dependent transcriptional activity were suppressed in jnk1 or jnk2 knockout (jnk1(-/-) or jnk2(-/-)) cells. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-97405 |
Thr81 |
APAPAAPtPAAPAPA |
Homo sapiens |
|
pmid |
sentence |
12531896 |
Wr1065 activates the jnk (c-jun n-terminal kinase), decreases complex formation between p53 and inactive jnk, and phosphorylates p53 at thr-81, a known site of phosphorylation by jnk. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-59812 |
|
|
Homo sapiens |
|
pmid |
sentence |
9724739 |
Activated jnk phosphorylates p53 |
|
Publications: |
3 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML |
+ |
STK17A | up-regulates
phosphorylation
|
TP53 |
0.29 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-153532 |
Ser20 |
PLSQETFsDLWKLLP |
Homo sapiens |
B-lymphocyte |
pmid |
sentence |
17339337 |
Genetic and biochemical studies have shown that ser20 phosphorylation in the transactivation domain of p53 mediates p300-catalyzed dna-dependent p53 acetylation and b-cell tumor suppression. a cell-free ser20 phosphorylation site assay was used to identify a broad range of calcium calmodulin kinase superfamily members, including chk2, chk1, dapk-1, dapk-3, drak-1, and ampk, as ser20 kinases. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
DUSP26 | down-regulates
dephosphorylation
|
TP53 |
0.374 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-166258 |
Ser20 |
PLSQETFsDLWKLLP |
Homo sapiens |
|
pmid |
sentence |
20562916 |
We found that dusp26 promotes the resistance of human neuroblastoma to doxorubicin-induced apoptosis by acting as a p53 phosphatase to downregulate p53 tumor suppressor function in neuroblastoma cells. / we found that dusp26 binds to p53 and dephosphorylates p53 at ser20 and ser37. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-166262 |
Ser37 |
NVLSPLPsQAMDDLM |
Homo sapiens |
|
pmid |
sentence |
20562916 |
We found that dusp26 promotes the resistance of human neuroblastoma to doxorubicin-induced apoptosis by acting as a p53 phosphatase to downregulate p53 tumor suppressor function in neuroblastoma cells. / we found that dusp26 binds to p53 and dephosphorylates p53 at ser20 and ser37. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
DAPK1 | up-regulates
phosphorylation
|
TP53 |
0.575 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-153487 |
Ser20 |
PLSQETFsDLWKLLP |
Homo sapiens |
|
pmid |
sentence |
17339337 |
A cell-free ser(20) phosphorylation site assay was used to identify a broad range of calcium calmodulin kinase superfamily members, including chk2, chk1, dapk-1, dapk-3, drak-1, and ampk, as ser(20) kinases.Evaluation of these calcium calmodulin kinase superfamily members as candidate ser(20) kinases in vivo has shown that only chk1 or dapk-1 can stimulate p53 transactivation and induce ser(20) phosphorylation of p53. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-153491 |
Thr18 |
EPPLSQEtFSDLWKL |
Homo sapiens |
B-lymphocyte |
pmid |
sentence |
17339337 |
Dna damage-activated protein kinases like chk1/2 modify the box-i domain of p53 at thr18 and ser20 (46) by an allosteric mechanism (10). |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
AURKA | down-regulates
phosphorylation
|
TP53 |
0.77 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-129809 |
Ser215 |
DRNTFRHsVVVPYEP |
Homo sapiens |
|
pmid |
sentence |
15469940 |
Here we show that p53 is phosphorylated by the mitotic kinase aurora-a at serine 215. Unlike most identified phosphorylation sites of p53 that positively associate with p53 function (brooks, c. L., and gu, w. (2003) curr. Opin. Cell biol. 15, 164-171), the phosphorylation of p53 by aurora-a at ser-215 abrogates p53 dna binding and transactivation activity. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CDK5/CDK5R1 | up-regulates activity
phosphorylation
|
TP53 |
0.57 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-250674 |
Ser315 |
LPNNTSSsPQPKKKP |
Rattus norvegicus |
PC-12 Cell |
pmid |
sentence |
12064478 |
the present study it is shown that in apoptotic PC12 cells the levels of p53 and Cdk5 increase concomitantly. Further, Cdk5/p25 effectively phosphorylates recombinant p53 in vitro. Transient transfection of Cdk5/p25 into cells results in an increase in p53 levels, as well as the expression of the p53-responsive genes p21 and Bax. Furthermore, evidence is provided that increased Cdk5 activity increases p53 transcriptional activity significantly, suggesting that p53 is modulated in situ by Cdk5. |
|
Publications: |
1 |
Organism: |
Rattus Norvegicus |
+ |
CDK2 | up-regulates activity
phosphorylation
|
TP53 |
0.867 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-119379 |
Ser315 |
LPNNTSSsPQPKKKP |
Homo sapiens |
|
pmid |
sentence |
24173284 |
The N-terminus of E2F1 can interact directly with a region towards the C-terminus of p53, resulting in increased nuclear retention of p53 and p53-mediated transcription and apoptosis. This is inhibited by competition between p53 and cyclin A at the binding site within E2F19,10. The interaction between p53 and E2F1 is enhanced by phosphorylation of p53 on Ser315, a residue within the E2F1 binding region that is phosphorylated by cell cycle kinases such as cdk1, cdk2, cdk9 and Aurora kinase A |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
AURKA | up-regulates activity
phosphorylation
|
TP53 |
0.77 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-120836 |
Ser315 |
LPNNTSSsPQPKKKP |
Homo sapiens |
|
pmid |
sentence |
24173284 |
The N-terminus of E2F1 can interact directly with a region towards the C-terminus of p53, resulting in increased nuclear retention of p53 and p53-mediated transcription and apoptosis. This is inhibited by competition between p53 and cyclin A at the binding site within E2F19,10. The interaction between p53 and E2F1 is enhanced by phosphorylation of p53 on Ser315, a residue within the E2F1 binding region that is phosphorylated by cell cycle kinases such as cdk1, cdk2, cdk9 and Aurora kinase A |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CDK9 | up-regulates activity
phosphorylation
|
TP53 |
0.551 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-145311 |
Ser315 |
LPNNTSSsPQPKKKP |
Homo sapiens |
|
pmid |
sentence |
24173284 |
The N-terminus of E2F1 can interact directly with a region towards the C-terminus of p53, resulting in increased nuclear retention of p53 and p53-mediated transcription and apoptosis. This is inhibited by competition between p53 and cyclin A at the binding site within E2F19,10. The interaction between p53 and E2F1 is enhanced by phosphorylation of p53 on Ser315, a residue within the E2F1 binding region that is phosphorylated by cell cycle kinases such as cdk1, cdk2, cdk9 and Aurora kinase A |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CDK1 | up-regulates activity
phosphorylation
|
TP53 |
0.597 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-167779 |
Ser315 |
LPNNTSSsPQPKKKP |
Homo sapiens |
|
pmid |
sentence |
24173284 |
The N-terminus of E2F1 can interact directly with a region towards the C-terminus of p53, resulting in increased nuclear retention of p53 and p53-mediated transcription and apoptosis. This is inhibited by competition between p53 and cyclin A at the binding site within E2F19,10. The interaction between p53 and E2F1 is enhanced by phosphorylation of p53 on Ser315, a residue within the E2F1 binding region that is phosphorylated by cell cycle kinases such as cdk1, cdk2, cdk9 and Aurora kinase A |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-84256 |
Ser315 |
LPNNTSSsPQPKKKP |
Homo sapiens |
|
pmid |
sentence |
24173284 |
The N-terminus of E2F1 can interact directly with a region towards the C-terminus of p53, resulting in increased nuclear retention of p53 and p53-mediated transcription and apoptosis. This is inhibited by competition between p53 and cyclin A at the binding site within E2F19,10. The interaction between p53 and E2F1 is enhanced by phosphorylation of p53 on Ser315, a residue within the E2F1 binding region that is phosphorylated by cell cycle kinases such as cdk1, cdk2, cdk9 and Aurora kinase A |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, IDH-TET in AML, KIT in AML |
+ |
CyclinA2/CDK2 | up-regulates
phosphorylation
|
TP53 |
0.803 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-217300 |
Ser315 |
LPNNTSSsPQPKKKP |
Homo sapiens |
|
pmid |
sentence |
14640983 |
We used non-radioactive electrophoretic mobility shift assays to show that c-terminal phosphorylation of p53 protein by cdk2/cyclin a on ser315 or by pkc on ser378 can efficiently stimulate p53 binding to dna in vitro. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CDC14A | down-regulates activity
dephosphorylation
|
TP53 |
0.411 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-248828 |
Ser315 |
LPNNTSSsPQPKKKP |
Homo sapiens |
|
pmid |
sentence |
10644693 |
The human Cdc14 phosphatases interact with and dephosphorylate the tumor suppressor protein p53|. Furthermore, the hCdc14 phosphatases were found to dephosphorylate p53 specifically at the p34Cdc2/clb phosphorylation site (p53-phosphor-Ser315)|Earlier studies showed that Ser315 phosphorylation increases the sequence-specific DNA binding capacity of p53, suggesting that Ser315 phosphorylation is an activating modification |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CDC14B | down-regulates activity
dephosphorylation
|
TP53 |
0.338 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-248332 |
Ser315 |
LPNNTSSsPQPKKKP |
Homo sapiens |
|
pmid |
sentence |
10644693 |
The human Cdc14 phosphatases interact with and dephosphorylate the tumor suppressor protein p53|. Furthermore, the hCdc14 phosphatases were found to dephosphorylate p53 specifically at the p34Cdc2/clb phosphorylation site (p53-phosphor-Ser315)|Earlier studies showed that Ser315 phosphorylation increases the sequence-specific DNA binding capacity of p53, suggesting that Ser315 phosphorylation is an activating modification |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
GSK3B | up-regulates activity
phosphorylation
|
TP53 |
0.717 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251258 |
Ser33 |
LPENNVLsPLPSQAM |
Homo sapiens |
|
pmid |
sentence |
11483158 |
Glycogen synthase kinase3 beta phosphorylates serine 33 of p53 and activates p53's transcriptional activity. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, AML_TRIPLETS, FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, Triple mutant AML |
+ |
CAK complex |
phosphorylation
|
TP53 |
0.446 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-269326 |
Ser33 |
LPENNVLsPLPSQAM |
Homo sapiens |
|
pmid |
sentence |
9372954 |
We have mapped a major site of phosphorylation by cak to ser-33 of p53 and have demonstrated as well that p53 is phosphorylated at this site in vivo. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CDK9 |
phosphorylation
|
TP53 |
0.551 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-145315 |
Ser33 |
LPENNVLsPLPSQAM |
Homo sapiens |
|
pmid |
sentence |
16552184 |
Here, we report for the first time that cyclin dependent kinase 9, whose well-known substrate is rna polymerase ii, can also phosphorylate p53. Specifically, ser33 on the n-terminus and, ser315 and ser392 on the c-terminus of p53 were found to be phosphorylated. The precise biological role of this phosphorylation remains to be elucidated. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CDK7 |
phosphorylation
|
TP53 |
0.47 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-53311 |
Ser33 |
LPENNVLsPLPSQAM |
Homo sapiens |
|
pmid |
sentence |
9372954 |
We have mapped a major site of phosphorylation by cak to ser-33 of p53 and have demonstrated as well that p53 is phosphorylated at this site in vivo. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MAPK13 | up-regulates
phosphorylation
|
TP53 |
0.443 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-72687 |
Ser33 |
LPENNVLsPLPSQAM |
Homo sapiens |
MCF-7 Cell |
pmid |
sentence |
10581258 |
In mcf-7 cells, p38 kinase activated p53 more effectively than other members of the ras pathway. p53 and p38 kinase exist in the same physical complex, and co-expression of p38 stabilized p53 protein. In vitro, p38 kinase phosphorylated p53 at ser33 and ser46, a newly identified site. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-72691 |
Ser46 |
AMDDLMLsPDDIEQW |
Homo sapiens |
|
pmid |
sentence |
10581258 |
In mcf-7 cells, p38 kinase activated p53 more effectively than other members of the ras pathway. p53 and p38 kinase exist in the same physical complex, and co-expression of p38 stabilized p53 protein. In vitro, p38 kinase phosphorylated p53 at ser33 and ser46, a newly identified site. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
PPP2CB | up-regulates quantity by stabilization
dephosphorylation
|
TP53 |
0.412 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-248584 |
Ser37 |
NVLSPLPsQAMDDLM |
Homo sapiens |
|
pmid |
sentence |
14712210 |
Phosphorylation of p53 at serine 37 is important for transcriptional activity and regulation in response to DNA damage| Furthermore, in vitro phosphatase assays show that PP2A dephosphorylates p53 at S37. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-248583 |
Thr55 |
DDIEQWFtEDPGPDE |
Homo sapiens |
|
pmid |
sentence |
17245430 |
A specific PP2A regulatory subunit, B56gamma, mediates DNA damage-induced dephosphorylation of p53 at Thr55| In this study, we reported that the specific B regulatory subunits of PP2A B56gamma1 and B56gamma3 mediate dephosphorylation of p53 at Thr55. Ablation of the B56gamma protein by RNAi, which abolishes the Thr55 dephosphorylation in response to DNA damage, reduces p53 stabilization, Bax expression and cell apoptosis |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
PPP2CA | down-regulates activity
dephosphorylation
|
TP53 |
0.573 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-248619 |
Ser37 |
NVLSPLPsQAMDDLM |
Homo sapiens |
|
pmid |
sentence |
14712210 |
Phosphorylation of p53 at serine 37 is important for transcriptional activity and regulation in response to DNA damage| Furthermore, in vitro phosphatase assays show that PP2A dephosphorylates p53 at S37. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MAPKAPK5 | up-regulates
phosphorylation
|
TP53 |
0.751 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-152847 |
Ser37 |
NVLSPLPsQAMDDLM |
Homo sapiens |
Skin Cancer Cell |
pmid |
sentence |
17254968 |
Furthermore, we show that prak activates p53 by direct phosphorylation. prak phosphorylates p53 at ser37 |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-152850 |
|
|
Homo sapiens |
Skin Cancer Cell |
pmid |
sentence |
17254968 |
Furthermore, we show that prak activates p53 by direct phosphorylation. We propose that phosphorylation of p53 by prak following activation of p38 mapk by ras plays an important role in ras-induced senescence and tumor suppression. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
CAK complex | up-regulates
phosphorylation
|
TP53 |
0.446 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-269327 |
Ser371 |
AHSSHLKsKKGQSTS |
Homo sapiens |
|
pmid |
sentence |
9315650 |
The cdk7-cych-p36 complex of transcription factor iih phosphorylates p53, enhancing its sequence-specific dna binding activity in vitro. serines 371, 376, 378, and 392 may be the potential sites for this kinase. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-269328 |
Ser376 |
LKSKKGQsTSRHKKL |
Homo sapiens |
|
pmid |
sentence |
9315650 |
The cdk7-cych-p36 complex of transcription factor iih phosphorylates p53, enhancing its sequence-specific dna binding activity in vitro. serines 371, 376, 378, and 392 may be the potential sites for this kinase. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-269325 |
Ser378 |
SKKGQSTsRHKKLMF |
Homo sapiens |
|
pmid |
sentence |
9315650 |
The cdk7-cych-p36 complex of transcription factor iih phosphorylates p53, enhancing its sequence-specific dna binding activity in vitro. serines 371, 376, 378, and 392 may be the potential sites for this kinase. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-269324 |
Ser392 |
FKTEGPDsD |
Homo sapiens |
|
pmid |
sentence |
9315650 |
The cdk7-cych-p36 complex of transcription factor iih phosphorylates p53, enhancing its sequence-specific dna binding activity in vitro. serines 371, 376, 378, and 392 may be the potential sites for this kinase. |
|
Publications: |
4 |
Organism: |
Homo Sapiens |
+ |
PRKCA | up-regulates activity
phosphorylation
|
TP53 |
0.448 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-248999 |
Ser371 |
AHSSHLKsKKGQSTS |
in vitro |
|
pmid |
sentence |
9571186 |
Here, we demonstrate that cotransfection of p53 with either PKC alpha or PKC zeta increases p53's transcriptional activity. Mutagenesis of p53 indicates that serine 371 is the major site for phosphorylation by PKC alpha in vitro. |
|
Publications: |
1 |
Organism: |
In Vitro |
+ |
CDK7 | up-regulates
phosphorylation
|
TP53 |
0.47 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-51280 |
Ser371 |
AHSSHLKsKKGQSTS |
Homo sapiens |
|
pmid |
sentence |
9315650 |
The cdk7-cych-p36 complex of transcription factor iih phosphorylates p53, enhancing its sequence-specific dna binding activity in vitro. serines 371, 376, 378, and 392 may be the potential sites for this kinase. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-51284 |
Ser376 |
LKSKKGQsTSRHKKL |
Homo sapiens |
|
pmid |
sentence |
9315650 |
The cdk7-cych-p36 complex of transcription factor iih phosphorylates p53, enhancing its sequence-specific dna binding activity in vitro. serines 371, 376, 378, and 392 may be the potential sites for this kinase. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-51288 |
Ser378 |
SKKGQSTsRHKKLMF |
Homo sapiens |
|
pmid |
sentence |
9315650 |
The cdk7-cych-p36 complex of transcription factor iih phosphorylates p53, enhancing its sequence-specific dna binding activity in vitro. serines 371, 376, 378, and 392 may be the potential sites for this kinase. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-51292 |
Ser392 |
FKTEGPDsD |
Homo sapiens |
|
pmid |
sentence |
9315650 |
The cdk7-cych-p36 complex of transcription factor iih phosphorylates p53, enhancing its sequence-specific dna binding activity in vitro. serines 371, 376, 378, and 392 may be the potential sites for this kinase. |
|
Publications: |
4 |
Organism: |
Homo Sapiens |
+ |
CyclinA2/CDK2 |
phosphorylation
|
TP53 |
0.803 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-250751 |
Ser392 |
FKTEGPDsD |
in vitro |
|
pmid |
sentence |
10884347 |
Our previous data has shown that cyclin A-cdk2 is the major enzyme responsible for modifying p53 at Ser315 in vivo after irradiation damage and in this report we dissect the mechanism of cyclinA-cdk2 binding to and phosphorylation of p53. |
|
Publications: |
1 |
Organism: |
In Vitro |
+ |
CDK9 | up-regulates
phosphorylation
|
TP53 |
0.551 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-201935 |
Ser392 |
FKTEGPDsD |
Homo sapiens |
|
pmid |
sentence |
23603988 |
We recently demonstrated that through their physical interaction, cdk9 phosphorylates p53 on ser-392, leading to p53 stability and accumulation |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CDK9 | up-regulates quantity by stabilization
phosphorylation
|
TP53 |
0.551 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-201931 |
Ser392 |
FKTEGPDsD |
Homo sapiens |
|
pmid |
sentence |
23603988 |
We recently demonstrated that through their physical interaction, cdk9 phosphorylates p53 on ser-392, leading to p53 stability and accumulation |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CSNK2A1 | up-regulates activity
phosphorylation
|
TP53 |
0.654 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-250967 |
Ser392 |
FKTEGPDsD |
Homo sapiens |
HeLa-S3 Cell |
pmid |
sentence |
10747897 |
Furthermore, we demonstrate that anisomycin- and tumor necrosis factor-alpha-induced phosphorylation of p53 at Ser-392, which is important for the transcriptional activity of this growth suppressor protein, requires p38 MAP kinase and CK2 activities. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
EIF2AK2 | up-regulates
phosphorylation
|
TP53 |
0.552 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-68033 |
Ser392 |
FKTEGPDsD |
Homo sapiens |
|
pmid |
sentence |
10348343 |
The double-stranded rna activated protein kinase pkr physically associates with the tumor suppressor p53 protein and phosphorylates human p53 on serine 392 in vitro. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
DYRK2 | up-regulates activity
phosphorylation
|
TP53 |
0.658 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-275578 |
Ser46 |
AMDDLMLsPDDIEQW |
|
|
pmid |
sentence |
19965871 |
Phosphorylation of p53 at Ser-46 is indispensable for the commitment to apoptotic cell death. |Upon exposure to genotoxic stress, ATM phosphorylates DYRK2 at Thr-33 and Ser-369, which enables DYRK2 to escape from degradation by dissociation from MDM2 and to induce the kinase activity toward p53 at Ser-46 in the nucleus. |
|
Publications: |
1 |
+ |
PRKCD | up-regulates
phosphorylation
|
TP53 |
0.663 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-143382 |
Ser46 |
AMDDLMLsPDDIEQW |
Homo sapiens |
|
pmid |
sentence |
16377624 |
Here, we show that the pro-apoptotic kinase, protein kinase c delta (pkcdelta), is involved in phosphorylation of p53 on ser(46). pkcdelta potentiates p53-dependent apoptosis by ser(46) phosphorylation in response to genotoxic stress. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
HIPK2 | up-regulates
phosphorylation
|
TP53 |
0.79 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-151930 |
Ser46 |
AMDDLMLsPDDIEQW |
Homo sapiens |
|
pmid |
sentence |
17210684 |
Based on all these observations, it is legitimate to suggest that axin and daxx seem to adopt both parallel routes and a convergent means to activate p53. In either case, hipk2 seems to be the protein kinase that catalyzes the ser46 phosphorylation. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Cell cycle: G2/M phase transition |
+ |
DYRK2 | up-regulates
phosphorylation
|
TP53 |
0.658 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-153544 |
Ser46 |
AMDDLMLsPDDIEQW |
Homo sapiens |
|
pmid |
sentence |
17349958 |
Here, we demonstrate that the dual-specificity tyrosine-phosphorylation-regulated kinase 2 (dyrk2) directly phosphorylates p53 at ser46. these findings indicate that dyrk2 regulates p53 to induce apoptosis in response to dna damage. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CSNK2A1 | down-regulates activity
phosphorylation
|
TP53 |
0.654 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-250968 |
Thr155 |
DSTPPPGtRVRAMAI |
in vitro |
|
pmid |
sentence |
12628923 |
CK2 phosphoryl ates Thr155, which targets p53 to degradation by the Ub system. |
|
Publications: |
1 |
Organism: |
In Vitro |
+ |
TTK | up-regulates
phosphorylation
|
TP53 |
0.514 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-184931 |
Thr18 |
EPPLSQEtFSDLWKL |
Homo sapiens |
|
pmid |
sentence |
19332559 |
Ttk/hmps1 mediates the p53-dependent postmitotic checkpoint by phosphorylating p53 at thr18. phosphorylation at thr18 enhances p53-dependent activation of not only p21 but also lats2, two mediators of the postmitotic checkpoint. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
VRK1 | up-regulates
phosphorylation
|
TP53 |
0.538 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-81222 |
Thr18 |
EPPLSQEtFSDLWKL |
Homo sapiens |
HeLa Cell |
pmid |
sentence |
10951572 |
Vrk1 phosphorylates murine p53 in threonine 18. This threonine is within the p53 hydrophobic loop (residues 13-23) required for the interaction of p53 with the cleft of its inhibitor mdm-2. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
PPP2CA | up-regulates quantity by stabilization
dephosphorylation
|
TP53 |
0.573 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-248618 |
Thr55 |
DDIEQWFtEDPGPDE |
Homo sapiens |
|
pmid |
sentence |
17245430 |
A specific PP2A regulatory subunit, B56gamma, mediates DNA damage-induced dephosphorylation of p53 at Thr55| In this study, we reported that the specific B regulatory subunits of PP2A B56gamma1 and B56gamma3 mediate dephosphorylation of p53 at Thr55. Ablation of the B56gamma protein by RNAi, which abolishes the Thr55 dephosphorylation in response to DNA damage, reduces p53 stabilization, Bax expression and cell apoptosis |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
GRK5 | down-regulates
phosphorylation
|
TP53 |
0.379 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-163707 |
Thr55 |
DDIEQWFtEDPGPDE |
Homo sapiens |
|
pmid |
sentence |
20124405 |
Grk5, but not grk2 or grk6, phosphorylates p53 at thr-55, which promotes the degradation of p53, leading to inhibition of p53-dependent apoptotic response to genotoxic damage. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
PPP2R5C | up-regulates quantity by stabilization
dephosphorylation
|
TP53 |
0.594 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-268154 |
Thr55 |
DDIEQWFtEDPGPDE |
Homo sapiens |
U2-OS Cell |
pmid |
sentence |
17245430 |
Ablation of the B56gamma protein by RNAi, which abolishes the Thr55 dephosphorylation in response to DNA damage, reduces p53 stabilization, Bax expression and cell apoptosis. To investigate the molecular mechanisms, we have shown that the endogenous B56gamma protein level and association with p53 increase after DNA damage. Finally, we demonstrate that Thr55 dephosphorylation is required for B56gamma3-mediated inhibition of cell proliferation and cell transformation. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TAF1 | down-regulates
phosphorylation
|
TP53 |
0.668 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-123651 |
Thr55 |
DDIEQWFtEDPGPDE |
Homo sapiens |
|
pmid |
sentence |
15053879 |
Phosphorylation on thr-55 by taf1 mediates degradation of p53 |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MAPK8 | up-regulates quantity by stabilization
phosphorylation
|
TP53 |
0.789 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-106542 |
Thr81 |
APAPAAPtPAAPAPA |
Homo sapiens |
HEK-293 Cell |
pmid |
sentence |
11283254 |
Jnk phosphorylated p53 at t81 in response to dna damage and stress-inducing agents, as determined by phospho-specific antibodies to t81 . Jun NH2-terminal kinase phosphorylation of p53 on Thr-81 is important for p53 stabilization and transcriptional activities in response to stress. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML |
+ |
SRC | down-regulates quantity by destabilization
phosphorylation
|
TP53 |
0.54 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-276668 |
Tyr126 |
AKSVTCTySPALNKM |
Homo sapiens |
HEK-293T Cell |
pmid |
sentence |
25071020 |
We recently found that ISGylation of the p53 tumor suppressor is an important novel mechanism to control its stability. Here we identified that Isg15-dependent regulation of p53 can be enhanced by different oncogenes. We further show that the Src-mediated phosphorylation of p53 on Tyr126 and Tyr220 has a positive effect on p53 ISGylation by enhancing Herc5 binding. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-276669 |
Tyr220 |
RHSVVVPyEPPEVGS |
Homo sapiens |
HEK-293T Cell |
pmid |
sentence |
25071020 |
We recently found that ISGylation of the p53 tumor suppressor is an important novel mechanism to control its stability. Here we identified that Isg15-dependent regulation of p53 can be enhanced by different oncogenes. We further show that the Src-mediated phosphorylation of p53 on Tyr126 and Tyr220 has a positive effect on p53 ISGylation by enhancing Herc5 binding. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
NEK10 | up-regulates activity
phosphorylation
|
TP53 |
0.259 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-273881 |
Tyr327 |
KKPLDGEyFTLQIRG |
Homo sapiens |
|
pmid |
sentence |
32561851 |
Here, we describe a function for NEK10 in the regulation of p53 transcriptional activity through tyrosine phosphorylation. NEK10 loss increases cellular proliferation by modulating the p53-dependent transcriptional output. NEK10 directly phosphorylates p53 on Y327, revealing NEK10's unexpected substrate specificity. A p53 mutant at this site (Y327F) acts as a hypomorph, causing an attenuated p53-mediated transcriptional response. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
p38 | up-regulates
phosphorylation
|
TP53 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-270126 |
|
|
Homo sapiens |
Skin Cancer Cell |
pmid |
sentence |
17254968 |
We show that prak activates p53 by direct phosphorylation. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
PARP1 | up-regulates activity
relocalization
|
TP53 |
0.576 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-261321 |
|
|
Homo sapiens |
|
pmid |
sentence |
17891139 |
We identify the major poly(ADP-ribosyl)ated sites of p53 by PARP-1 and find that PARP-1-mediated poly(ADP-ribosyl)ation blocks the interaction between p53 and the nuclear export receptor Crm1, resulting in nuclear accumulation of p53. These findings molecularly link PARP-1 and p53 in the DNA-damage response, providing the mechanism for how p53 accumulates in the nucleus in response to DNA damage.|PARP-1 is super-activated by binding to damaged DNA, and poly(ADP-ribosyl)ates p53. Poly(ADP-ribosyl)ation probably induces a structural change that mask the NES, and thus Crm1 can no longer target p53 to the nuclear export machinery, resulting in accumulation of p53 in the nucleus. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML, FLT3-ITD signaling, Mitochondrial Control of Apoptosis |
+ |
EIF5A | up-regulates quantity by expression
transcriptional regulation
|
TP53 |
0.372 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-266375 |
|
|
Chlorocebus aethiops |
|
pmid |
sentence |
15371445 |
eIF5A regulated p53 protein expression. Further analysis by reverse transcription PCR showed eIF5A-activated p53 transcription. The effect of eIF5A on p53 transcriptional activity was further demonstrated by the increasing expressions of p21 and Bax, well known target genes of p53. |
|
Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
+ |
TP53 | down-regulates activity
binding
|
ETS1 |
0.547 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-254087 |
|
|
Homo sapiens |
|
pmid |
sentence |
14586398 |
We demonstrate that p53 and ets-1 coregulate TXSA in an antagonistic and inter-related manner, with ets-1 being a potent transcriptional activator and p53 inhibiting ets-1-dependent transcription. We show that ets-1 and p53 associate physically in vitro and in vivo and that their interaction, rather than a direct binding of p53 to the TXSA promoter, is required for transcriptional repression of TXSA by wild-type p53. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
ANKRD11 | up-regulates activity
binding
|
TP53 |
0.313 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-266734 |
|
|
Homo sapiens |
MCF-7 Cell |
pmid |
sentence |
18840648 |
Ankyrin repeat domain 11, ANKRD11 (also known as ANR11 or ANCO1), was found to be a novel p53-interacting protein that enhanced the transcriptional activity of p53. In addition, ANKRD11 itself was found to be a novel p53 target gene. These findings demonstrate a role for ANKRD11 as a p53 coactivator and suggest the involvement of ANKRD11 in a regulatory feedback loop with p53. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
C10orf90 | up-regulates quantity by stabilization
polyubiquitination
|
TP53 |
0.471 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-272142 |
|
|
Homo sapiens |
U2-OS Cell |
pmid |
sentence |
24240685 |
The E3 activity of FATS is required for promoting p53 stability and activation in response to DNA damage.FATS is an E2-independent ubiquitin ligase that stabilizes p53 and promotes its activation in response to DNA damage. Here, we show that FATS acts as a p53 activator by inhibiting Mdm2 binding to p53 and stimulating non-proteolytic polyubiquitination of p53. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
UBE4B | down-regulates quantity by destabilization
polyubiquitination
|
TP53 |
0.405 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-271907 |
|
|
Homo sapiens |
NCI-H1299 Cell |
pmid |
sentence |
21317885 |
We show that ubiquitination factor E4B (UBE4B), an E3 and E4 ubiquitin ligase, physically interacts with p53 and Hdm2 (also known as Mdm2 in mice). UBE4B promotes p53 polyubiquitination and degradation and inhibits p53-dependent transactivation and apoptosis. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates
|
Cell_death |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-256664 |
|
|
Homo sapiens |
|
pmid |
sentence |
24212651 |
P53 is a nuclear transcription factor with a pro-apoptotic function |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
BID |
0.499 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-140248 |
|
|
Mus musculus |
|
pmid |
sentence |
16151013 |
Bid is a p53 primary-response gene. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
Pathways: | Mitochondrial Control of Apoptosis |
+ |
TP53 | down-regulates activity
binding
|
BCL2 |
0.739 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-99712 |
|
|
Homo sapiens |
|
pmid |
sentence |
19007744 |
Mechanistic insights into the mitochondrial function of wtp53 came when it was realized that mitochondrially translocated p53 interacts directly with members of the Bcl-2 family, which are central in governing the induction of mitochondrial outer membrane permeabilization. In response to stress, wtp53 interacts with and neutralizes the anti-apoptotic members Bcl-xL and Bcl-2. This interaction stimulates MOMP and subsequent apoptosis |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, DNMT3A in AML, KIT in AML, miRNA in AML, AML_TRIPLETS, Colorectal Carcinoma, FLT3-ITD signaling, Mitochondrial Control of Apoptosis, Malignant Melanoma, Triple mutant AML, NPM1_new, Non-small-cell lung cancer (NSCLC), p53 in cancer |
+ |
TP53 | down-regulates
binding
|
BIRC5 |
0.544 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-111971 |
|
|
Homo sapiens |
|
pmid |
sentence |
11714700 |
This study identifies the anti-apoptotic survivin gene as a p53-repressed gene;notably, survivin repression by p53 is shown to be distinct from p53-dependent growth arrest. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates
binding
|
BAX |
0.743 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-121895 |
|
|
Homo sapiens |
|
pmid |
sentence |
14963330 |
Tp53 directly activated the proapoptotic bcl-2 protein bax in the absence of other proteins to permeabilize mitochondria and engage the apoptotic program |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-140242 |
|
|
Homo sapiens |
|
pmid |
sentence |
16151013 |
P53 also accumulates in the cytoplasm where it directly activates bax to promote mitochondrial outer membrane permeabilization. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, FLT3-ITD signaling, Mitochondrial Control of Apoptosis, Malignant Melanoma, p53 in cancer |
+ |
BAD | up-regulates activity
binding
|
TP53 |
0.335 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-149815 |
|
|
Homo sapiens |
NCI-H1299 Cell |
pmid |
sentence |
17000778 |
We also demonstrate that bad physically interacts with cytoplasmic p53. bad is able to direct p53 to the mitochondria and forms a p53/bad complex at the mitochondria. the mitochondrial p53/bad complex promotes apoptosis |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML, FLT3-ITD signaling, Mitochondrial Control of Apoptosis, Malignant Melanoma |
+ |
TP53 | up-regulates
binding
|
CBP/p300 |
0.909 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-66956 |
|
|
Homo sapiens |
|
pmid |
sentence |
10207072 |
Both p53 and rela(p65) interact with the transcriptional coactivator proteins p300 and creb-binding protein (cbp), and we demonstrate that these results are consistent with competition for a limiting pool of p300/cbp complexes in vivo. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MAML1 | up-regulates
binding
|
TP53 |
0.315 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-180136 |
|
|
Homo sapiens |
|
pmid |
sentence |
18758483 |
Unexpectedly, however, emerging evidence implicate maml proteins as exciting key transcriptional co-activators in other signal transduction pathways including: muscle differentiation and myopathies (mef2c), tumor suppressor pathway (p53) and colon carcinoma survival (beta-catenin). |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Tissue: |
Muscle |
+ |
TP53 | up-regulates activity
binding
|
BAX |
0.743 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-178690 |
|
|
Homo sapiens |
|
pmid |
sentence |
14963330 |
Tp53 directly activated the proapoptotic bcl-2 protein bax in the absence of other proteins to permeabilize mitochondria and engage the apoptotic program |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, FLT3-ITD signaling, Mitochondrial Control of Apoptosis, Malignant Melanoma, p53 in cancer |
+ |
GMPS | up-regulates
binding
|
TP53 |
0.387 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-204409 |
|
|
Homo sapiens |
|
pmid |
sentence |
24462112 |
In response to genotoxic stress or nucleotide deprivation, gmps becomes nuclear and facilitates p53 stabilization by promoting its transfer from mdm2 to a gmps-usp7 deubiquitylation complex. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MLF1 | up-regulates
|
TP53 |
0.294 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-135943 |
|
|
Homo sapiens |
|
pmid |
sentence |
15861129 |
Mlf1 induces p53-dependent cell cycle arrest |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | down-regulates
|
Proliferation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255669 |
|
|
Homo sapiens |
Fibroblast |
pmid |
sentence |
7667317 |
P53 controls both the G2/M and the G1 cell cycle checkpoints and mediates reversible growth arrest in human fibroblasts |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, DNMT3A in AML, Onco-fusion proteins in AML, IDH-TET in AML, KIT in AML, miRNA in AML, NPM1 in AML, AML_TRIPLETS, Colorectal Carcinoma, EBV infection, FLT3-ITD in AML, FLT3-ITD signaling, Luminal Breast Cancer, Malignant Melanoma, Triple mutant AML, NPM1_new, Non-small-cell lung cancer (NSCLC), P38 Signaling, Prostate Cancer, Pancreatic ductal adenocarcinoma (PDA) |
+ |
SIRT1 | down-regulates quantity by destabilization
deacetylation
|
TP53 |
0.796 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-261562 |
|
|
Homo sapiens |
|
pmid |
sentence |
25280219 |
SIRT1 overexpression was associated with down-modulation of p53 activity in FLT3-ITD AML CD34+ cells. SIRT1 can negatively regulate p53 by deacetylating several lysine sites |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
ZNF365 |
0.295 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-272476 |
|
|
Homo sapiens |
|
pmid |
sentence |
23776040 |
Here, analysis of p53-regulated genes activated in the setting of telomere dysfunction identified Zfp365 (ZNF365 in humans) as a direct p53 target that promotes genome stability| Our study identified ZNF365 as a necessary target whose activation by p53 in the presence of critically short telomeres contributes to genomic stability. We provide evidence that loss of ZNF365 leads to increased expression of CFS and dysfunctional telomeres, aberrant sister telomere recombination, and increased aneuploidy |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
NUMB | up-regulates
|
TP53 |
0.531 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-168457 |
|
|
Homo sapiens |
|
pmid |
sentence |
20940030 |
Numb interacts with mdm2, and inhibits its ubiquitin-ligase function on tp53 (which in itself is inhibitory for tp53), thus numb activates (b) tp53. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates
|
Apoptosis |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255678 |
|
|
Homo sapiens |
|
pmid |
sentence |
24212651 |
P53 is a nuclear transcription factor with a pro-apoptotic function |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, DNMT3A in AML, Onco-fusion proteins in AML, KIT in AML, miRNA in AML, NPM1 in AML, AML_TRIPLETS, Colorectal Carcinoma, EBV infection, FLT3-ITD in AML, FLT3-ITD signaling, Mitochondrial Control of Apoptosis, Malignant Melanoma, Triple mutant AML, NPM1_new, P38 Signaling, p53 in cancer, Pancreatic ductal adenocarcinoma (PDA) |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
IL6 |
0.479 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255969 |
|
|
Homo sapiens |
Macrophage |
pmid |
sentence |
24737129 |
We have identified a novel role for p53 that is specific to the regulation of several pro-inflammatory genes in human macrophages, including IL-6, IL-8 and CXCL1. Importantly, NF-κB co-activation is essential for this regulation |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
BCLAF1 | up-regulates quantity by expression
transcriptional regulation
|
TP53 |
0.423 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-261568 |
|
|
Homo sapiens |
|
pmid |
sentence |
17938203 |
These results demonstrate that Btf positively regulates TP53 expression through CPE-TP53. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
NDRG1 |
0.509 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-129183 |
|
|
Homo sapiens |
|
pmid |
sentence |
15377670 |
We isolated a p53-regulated gene named ndrg1 (n-myc down-regulated gene 1). Its expression is induced by dna damage in a p53-dependent fashion. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
PMAIP1 |
0.69 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-76152 |
|
|
Homo sapiens |
|
pmid |
sentence |
10807576 |
Expression of noxa was dependent on p53. Noxa represent a mediator of p53-dependent apoptosis. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-118048 |
|
|
Homo sapiens |
|
pmid |
sentence |
14500851 |
P53 has the ability to activate transcription of various proapoptotic genes, including those encoding members of the bcl-2 family, such as the bh-3 only proteins bax, noxa, and puma pmaip1 may thus represent a mediator of tp53-dependent apoptosis. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
YY2 | up-regulates quantity by expression
transcriptional regulation
|
TP53 |
0.591 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-266213 |
|
|
Homo sapiens |
HeLa Cell |
pmid |
sentence |
15087442 |
YY2 activated the p53 promoter. However, in contrast to YY1, which represses the activity of c-Fos, YY2 increased the activity of the c-Fos promoter. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
FHIT | up-regulates
|
TP53 |
0.487 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-127915 |
|
|
Homo sapiens |
Lung Cancer Cell |
pmid |
sentence |
15313915 |
We found that this synergistic inhibition of tumor cell growth corresponded with the fhit-mediated inactivation of mdm2, which thereby blocked the association of mdm2 with p53, thus stabilizing the p53 protein. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Pancreatic ductal adenocarcinoma (PDA) |
+ |
TRIM39 | down-regulates quantity by destabilization
ubiquitination
|
TP53 |
0.358 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-272020 |
|
|
Homo sapiens |
NCI-H1299 Cell |
pmid |
sentence |
23213260 |
Furthermore, we show here that the Trim39 can directly bind and ubiquitylate p53 in vitro and in vivo, leading to p53 degradation. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
EGFR |
0.591 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255430 |
|
|
Homo sapiens |
|
pmid |
sentence |
10029407 |
p53 transcriptionally activates expression of the genes encoding epidermal growth factor receptor, matrix metalloproteinase (MMP)-2, cathepsin D, and thrombospondin-1 but represses expression of the genes encoding basic fibroblast growth factor and multidrug resistance-1. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML, Non-small-cell lung cancer (NSCLC), Pancreatic ductal adenocarcinoma (PDA) |
+ |
TP53 | up-regulates
|
RPS6KA1 |
0.365 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-124038 |
|
|
Homo sapiens |
|
pmid |
sentence |
15073170 |
Rather, p53 expression stimulates the serine/threonine kinase ribosomal s6 kinase 1 (rsk1), which in turn phosphorylates the p65 subunit of nf-kb. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | FLT3-ITD signaling |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
NR4A3 |
0.268 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-256200 |
|
|
Homo sapiens |
|
pmid |
sentence |
30455429 |
We showed that p53 directly bound the promoter of NR4A3 gene and induced its transcription. p53 transactivates the NR4A3 promoter in H1299 cells. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates
|
RPS6K |
0.365 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-252816 |
|
|
Homo sapiens |
|
pmid |
sentence |
15073170 |
Rather, p53 expression stimulates the serine/threonine kinase ribosomal s6 kinase 1 (rsk1), which in turn phosphorylates the p65 subunit of nf-kb. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | FLT3-ITD signaling |
+ |
TFAP2B | up-regulates quantity by stabilization
binding
|
TP53 |
0.341 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255422 |
|
|
Homo sapiens |
|
pmid |
sentence |
21556774 |
These data suggest that AP-2β enhances transactivation of p53 and regulates CRYAB transcription via p53. Further study demonstrated that AP-2β interacts with p53 and augments its protein stability. Taken together, our results indicate that AP-2β up-regulates the transcription of the CRYAB gene through stabilizing p53. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CBLB | up-regulates activity
|
TP53 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-261320 |
|
|
Homo sapiens |
MOLM-13 Cell |
pmid |
sentence |
27773928 |
We have also shown that the E3 ubiquitin ligase Cbl-b is crucial for activation of the p53 pathway through ubiquitinating and promoting degradation of Siva1, the E3 ubiquitin ligase targeting ARF, a positive regulator of p53. On the basis of our data presented in the study, we propose the model (Figure 2i) that Cbl-b negatively regulates Siva1 by ubiquitination and subsequent degradation of Siva1, which is followed by stabilization of ARF. This in turn downregulates MDM2, thereby promoting the induction of p53 and activation of its downstream targets. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, KIT in AML |
+ |
CREBBP | up-regulates activity
acetylation
|
TP53 |
0.91 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-261495 |
|
|
Homo sapiens |
|
pmid |
sentence |
25545885 |
C-terminal acetylation of p53 by p300/CBP and PCAF promotes an open conformation of p53 by preventing the occlusion of the DNA binding domain by the C-terminal tail. This enhances p53 transcriptional activity, leading to growth arrest and/or apoptosis |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | down-regulates quantity by repression
transcriptional regulation
|
BCL2 |
0.739 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-271677 |
|
|
|
|
pmid |
sentence |
10329733 |
P53 suppresses the activation of the Bcl-2 promoter by the Brn-3a POU family transcription factor. |
|
Publications: |
1 |
Pathways: | Acute Myeloid Leukemia, DNMT3A in AML, KIT in AML, miRNA in AML, AML_TRIPLETS, Colorectal Carcinoma, FLT3-ITD signaling, Mitochondrial Control of Apoptosis, Malignant Melanoma, Triple mutant AML, NPM1_new, Non-small-cell lung cancer (NSCLC), p53 in cancer |
+ |
CDKN2AIP | up-regulates
binding
|
TP53 |
0.392 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-147360 |
|
|
Homo sapiens |
|
pmid |
sentence |
16803988 |
In the nucleoplasm, carf interacts with p53 and enhances its function. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
CDKN1A |
0.873 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-29248 |
|
|
Homo sapiens |
|
pmid |
sentence |
7566157 |
The p21 gene is under the transcriptional control of p53 (ref. 5), suggesting that p21 might promote p53-dependent cell cycle arrest or apoptosis. p21cip1 is a cyclin-dependent kinase (cdk) inhibitor that is transcriptionally activated by p53 in response to dna damage. p53 then transcriptionally upregulates the expression of target genes, of which p21 is critical for inhibiting g1/s entry. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-173425 |
|
|
Homo sapiens |
|
pmid |
sentence |
21524151 |
P53 then transcriptionally upregulates the expression of target genes, of which p21 is critical for inhibiting G1/S entry. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-37145 |
|
|
Homo sapiens |
|
pmid |
sentence |
8242752 |
The ability of p53 to activate transcription from specific sequences suggests that genes induced by p53 may mediate its biological role as a tumor suppressor. Using a subtractive hybridization approach, we identified a gene, named WAF1, whose induction was associated with wild-type but not mutant p53 gene expression in a human brain tumor cell line. The WAF1 gene was localized to chromosome 6p21.2, and its sequence, structure, and activation by p53 was conserved in rodents. |
|
Publications: |
3 |
Organism: |
Homo Sapiens |
Tissue: |
Brain |
Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML, FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
FNTB |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-242353 |
|
|
Homo sapiens |
|
pmid |
sentence |
26469958 |
In this study, we provided evidence that p53 induces the expression of a group of enzymes of the MVA pathway including 3'-hydroxy-3'-methylglutaryl-coenzyme A reductase, MVA kinase, farnesyl diphosphate synthase and farnesyl diphosphate farnesyl transferase 1, in the human glioblastoma multiforme cell line, U343 cells, and in normal human astrocytes, NHAs. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | down-regulates quantity by repression
transcriptional regulation
|
HR |
0.348 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255436 |
|
|
Homo sapiens |
|
pmid |
sentence |
15489903 |
P53 may downregulate HR through multiple mechanisms including the reported associations with the Rad51 and Rad54 recombinases, and the BLM and WRN helicases. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
FNTA |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-242408 |
|
|
Homo sapiens |
|
pmid |
sentence |
26469958 |
In this study, we provided evidence that p53 induces the expression of a group of enzymes of the MVA pathway including 3'-hydroxy-3'-methylglutaryl-coenzyme A reductase, MVA kinase, farnesyl diphosphate synthase and farnesyl diphosphate farnesyl transferase 1, in the human glioblastoma multiforme cell line, U343 cells, and in normal human astrocytes, NHAs. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
UBE3A | down-regulates quantity by destabilization
polyubiquitination
|
TP53 |
0.672 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-272552 |
|
|
Homo sapiens |
|
pmid |
sentence |
9497376 |
E6AP and E6 together provide the E3-ubiquitin protein ligase activity in the transfer of ubiquitin to p53. In vitro studies have shown that E6AP can form a high energy thiolester bond with ubiquitin and, in the presence of E6, transfer ubiquitin to p53. In this study we have addressed the role of E6AP in vivo in the degradation of p53. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
KDM4B |
0.285 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-263729 |
|
|
Homo sapiens |
HCT-116 Cell |
pmid |
sentence |
28073943 |
KDM4B/JMJD2B is a p53 target gene that modulates the amplitude of p53 response after DNA damage. p53 directly regulates JMJD2B gene expression by binding to a canonical p53-consensus motif in the JMJD2B promoter. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
CRYAB |
0.483 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-253638 |
|
|
Homo sapiens |
|
pmid |
sentence |
21556774 |
Aberrant expression of CRYAB has been shown to be associated with several neurological diseases and malignant neoplasms. To identify transcriptional regulators of CRYAB expression, we examined its promoter for binding sites of transcription factors and identified four potential AP-2 binding sites in addition to a p53 binding site reported previously|Taken together, our results indicate that AP-2_ up-regulates the transcription of the CRYAB gene through stabilizing p53 |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates quantity
transcriptional regulation
|
PMS2 |
0.565 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-257604 |
|
|
Homo sapiens |
|
pmid |
sentence |
15781865 |
.... numerous potentially novel targets, including the DNA mismatch repair genes MLH1 and PMS2. Both of these genes were determined to be responsive to DNA damage and p53 activation in normal human fibroblasts, and have p53-response elements within their first intron. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
EP300 | down-regulates quantity by destabilization
polyubiquitination
|
TP53 |
0.909 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-271418 |
|
|
Homo sapiens |
|
pmid |
sentence |
12690203 |
P53 is stabilized by the binding of p300 to the oncoprotein E1A, suggesting that p300 regulates p53 degradation. Purified p300 exhibited intrinsic ubiquitin ligase activity that was inhibited by E1A. In vitro, p300 with MDM2 catalyzed p53 polyubiquitination, whereas MDM2 catalyzed p53 monoubiquitination. E1A expression caused a decrease in polyubiquitinated but not monoubiquitinated p53 in cells. Thus, generation of the polyubiquitinated forms of p53 that are targeted for proteasome degradation requires the intrinsic ubiquitin ligase activities of MDM2 and p300. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, p53 in cancer |
+ |
seliciclib | down-regulates
chemical inhibition
|
TP53 |
0.8 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-206577 |
|
|
Homo sapiens |
|
pmid |
sentence |
Other |
|
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
VHL | up-regulates quantity by stabilization
binding
|
TP53 |
0.464 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-256594 |
|
|
Homo sapiens |
HEK-293 Cell |
pmid |
sentence |
16678111 |
Here we found that pVHL directly associates with and stabilizes p53 by suppressing Mdm2-mediated ubiquitination and nuclear export of p53. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MDM2 | down-regulates quantity by destabilization
ubiquitination
|
TP53 |
0.968 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-80528 |
|
|
Homo sapiens |
|
pmid |
sentence |
10935507 |
Many posttranslational modifications of p53, such as phosphorylation, dephosphorylation, acetylation and ribosylation, have been shown to occur following cellular stress. Some of these modifications may activate the p53 protein, interfere with MDM2 binding and/or dictate cellular localization of p53. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-199371 |
|
|
Homo sapiens |
|
pmid |
sentence |
23150757 |
Dual Roles of MDM2 in the Regulation of p53: Ubiquitination Dependent and Ubiquitination Independent Mechanisms of MDM2 Repression of p53 Activity |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-196116 |
|
|
Homo sapiens |
|
pmid |
sentence |
22337874 |
The E3 ubiquitin ligase, MDM2, uses a dual-site mechanism to ubiquitinate and degrade the tumor suppressor protein p53, involving interactions with the N-terminal hydrophobic pocket and the acidic domain of MDM2. |
|
Publications: |
3 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, DNMT3A in AML, IDH-TET in AML, miRNA in AML, NPM1 in AML, FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, Luminal Breast Cancer, Malignant Melanoma, Triple mutant AML, NPM1_new, Prostate Cancer, p53 in cancer, Pancreatic ductal adenocarcinoma (PDA) |
+ |
USP10 | up-regulates quantity by stabilization
deubiquitination
|
TP53 |
0.648 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-260297 |
|
|
Homo sapiens |
H4 Neuroglioma Cell |
pmid |
sentence |
21962518 |
Since USP10 is known as a deubiquitinating protease of p53 (Yuan et al., 2010), inhibition of USP10 by spautin-1 may promote the degradation of p53. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
GADD45A |
0.647 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-201679 |
|
|
Homo sapiens |
|
pmid |
sentence |
23576563 |
P53 acetylated at k120 subsequently bound to the promoters of its target apoptotic genes, bax and gadd45, to promote their expression and lead to apoptosis. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
NLRC4 |
0.425 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255439 |
|
|
Homo sapiens |
|
pmid |
sentence |
15580302 |
Here we show that Ipaf, a human CED-4 homologue and an activator of caspase-1, is induced by p53. Overexpression of p53 by transfection in U2OS and A549 cells increased Ipaf mRNA levels. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
PIK3R3 | up-regulates activity
binding
|
TP53 |
0.301 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-261492 |
|
|
Homo sapiens |
HEK-293 Cell |
pmid |
sentence |
32606738 |
N this study, we aimed to explore the interaction of p55PIK with p53 and the role of p55PIK in regulating p53-dependent apoptosis in cancer cells. We found that p55PIK directly binds to the DBD domain of p53 via N24 domain. Moreover, the upregulation of p55PIK expression increases transcriptional levels of p53-dependent apoptosis-related genes including GADD45α, S100A9, MDM2 and AIP1. Furthermore, synthetic N24 translocated to nucleus can significantly inhibit cancer cell growth. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
TNFRSF10B |
0.634 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-113707 |
|
|
Homo sapiens |
|
pmid |
sentence |
14585074 |
Cd95l, cd95, and the trail death receptors are induced by the tumour suppressor p53 |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-138293 |
|
|
Homo sapiens |
|
pmid |
sentence |
15964798 |
Reduction in p53 expression also blocks p65 binding to the intronic region of the dr5 gene, indicating cooperation between p53 and p65 in dr5 expression. (articolo-abstract) |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
SIRT7 | down-regulates
deacetylation
|
TP53 |
0.514 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-160539 |
|
|
Homo sapiens |
|
pmid |
sentence |
18239138 |
We found that sirt7 interacts with p53 and efficiently deacetylates p53 in vitro, which corresponds to hyperacetylation of p53 in vivo. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | down-regulates quantity by repression
transcriptional regulation
|
SLC2A4 |
0.343 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-267465 |
|
|
Homo sapiens |
|
pmid |
sentence |
27692180 |
P53 regulates basal expression of AIF and SCO2 and facilitates oxidative phosphorylation. The expression of GLUT1, GLUT4, and HK2 is negatively regulated by p53, whereas TIGAR expression is induced by p53. The net result of p53-mediated regulation of these glycolytic enzymes is the suppression of glycolysis. In addition, p53 directly binds and inhibits G6PD activity and downregulates the pentose phosphate pathway. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Glycolysis and Gluconeogenesis |
+ |
TP53 | down-regulates quantity by repression
transcriptional regulation
|
AFP |
0.449 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-254482 |
|
|
Homo sapiens |
|
pmid |
sentence |
14522900 |
In this study, we found that a subset of ING family members strongly repressed human alpha-fetoprotein (AFP) promoter activity but stimulated the p21(WAF1) promoter in parallel experiments in the same cell type, similar to the effects of p53. Both ING1 and p53 were able to suppress AFP transcription and cause p21 induction |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
FAS |
0.589 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-62376 |
|
|
Homo sapiens |
Breast Cancer Cell |
pmid |
sentence |
9841917 |
In an attempt to understand how CD95 expression is regulated by p53, we identified a p53-responsive element within the first intron of the CD95 gene, as well as three putative elements within the promoter. The intronic element conferred transcriptional activation by p53 and cooperated with p53-responsive elements in the promoter of the CD95 gene. wt p53 bound to and transactivated the CD95 gene, |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Mitochondrial Control of Apoptosis |
+ |
RPS6KA4 | down-regulates
|
TP53 |
0.252 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-188334 |
|
|
Homo sapiens |
|
pmid |
sentence |
19797274 |
Mitogen- and stress-activated kinase 2 (msk2) inhibits the transcription factor p53, and we investigate here the mechanisms underlying this inhibition. In the absence of stress stimuli, msk2 selectively suppressed the expression of a subset of p53 target genes.Msk2 can also control the the transcriptional activity of p53 in a kinase-indipendent mannermsk2 can also control the the transcriptional activity of p53 in a kinase-indipendent manner |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
ANKRD11 |
0.313 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-266735 |
|
|
Homo sapiens |
MCF-7 Cell |
pmid |
sentence |
18840648 |
Ankyrin repeat domain 11, ANKRD11 (also known as ANR11 or ANCO1), was found to be a novel p53-interacting protein that enhanced the transcriptional activity of p53. In addition, ANKRD11 itself was found to be a novel p53 target gene. These findings demonstrate a role for ANKRD11 as a p53 coactivator and suggest the involvement of ANKRD11 in a regulatory feedback loop with p53. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
NfKb-p65/p50 | up-regulates quantity by expression
|
TP53 |
0.5 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-123602 |
|
|
Homo sapiens |
|
pmid |
sentence |
15044535 |
These results indicate that nf-kb actions occur upstream of p53 to regulate both p53 levels and activity. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, miRNA in AML, EBV infection, FLT3-ITD signaling, Pancreatic ductal adenocarcinoma (PDA) |
+ |
TP53 | down-regulates quantity by repression
transcriptional regulation
|
MGMT |
0.488 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255437 |
|
|
Homo sapiens |
Glioma Cell Line |
pmid |
sentence |
17564708 |
we observed that IFN-beta sensitized TMZ-resistant glioma cells with the unmethylated MGMT promoter and that the mechanism of action was possibly due to attenuation of MGMT expression via induction of TP53. In this context, IFN-beta inactivates MGMT via p53 gene induction and enhances the therapeutic efficacy to TMZ. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | down-regulates quantity by repression
transcriptional regulation
|
RLIM |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-268981 |
|
|
|
|
pmid |
sentence |
23650532 |
In the present study, we identified RLIM as a novel target of p53 and demonstrated that p53 repressed both mRNA and protein levels of RLIM. |
|
Publications: |
1 |
+ |
BRCC ubiquitin ligase complex |
ubiquitination
|
TP53 |
0.616 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-263210 |
|
|
Homo sapiens |
HEK-293 Cell |
pmid |
sentence |
14636569 |
However, since the same domain of p53 is also the target of ubiquitination by MDM2 protein, further in vivo experiments are required to demonstrate the biological relevance of p53 ubiquitination by BRCC.|The Extreme C Terminus of p53 Is Ubiquitinated by BRCC |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
SWI/SNF complex | up-regulates activity
binding
|
TP53 |
0.444 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-256285 |
|
|
Homo sapiens |
HEK-293T Cell |
pmid |
sentence |
11950834 |
Using genetic and biochemical approaches, we show that several subunits of the human SWI/SNF complex bind to the tumor suppressor protein p53 in vivo and in vitro.Molecular connection between p53 and the SWI/SNF complex implicates that (i) the SWI/SNF complex is necessary for p53-driven transcriptional activation, and (ii) the SWI/SNF complex plays an important role in p53-mediated cell cycle control. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
[5-[5-[5-(hydroxymethyl)-2-thiophenyl]-2-furanyl]-2-thiophenyl]methanol | up-regulates
chemical activation
|
TP53 |
0.8 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-184062 |
|
|
Homo sapiens |
|
pmid |
sentence |
19223463 |
Rita has been proposed to stabilize p53 by inhibiting the p53-hdm2 interaction. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
BAX |
0.743 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-33922 |
|
|
Homo sapiens |
|
pmid |
sentence |
7834749 |
Bax is a p53 primary-response gene, presumably involved in a p53-regulated pathway for induction of apoptosis |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, FLT3-ITD signaling, Mitochondrial Control of Apoptosis, Malignant Melanoma, p53 in cancer |
+ |
TP53 | down-regulates quantity by repression
transcriptional regulation
|
FGF2 |
0.452 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255431 |
|
|
Homo sapiens |
|
pmid |
sentence |
10029407 |
p53 transcriptionally activates expression of the genes encoding epidermal growth factor receptor, matrix metalloproteinase (MMP)-2, cathepsin D, and thrombospondin-1 but represses expression of the genes encoding basic fibroblast growth factor and multidrug resistance-1. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | down-regulates quantity by repression
transcriptional regulation
|
HK2 |
0.423 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-267466 |
|
|
Homo sapiens |
|
pmid |
sentence |
27692180 |
P53 regulates basal expression of AIF and SCO2 and facilitates oxidative phosphorylation. The expression of GLUT1, GLUT4, and HK2 is negatively regulated by p53, whereas TIGAR expression is induced by p53. The net result of p53-mediated regulation of these glycolytic enzymes is the suppression of glycolysis. In addition, p53 directly binds and inhibits G6PD activity and downregulates the pentose phosphate pathway. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Glycolysis and Gluconeogenesis |
+ |
MAPK10 | up-regulates
phosphorylation
|
TP53 |
0.616 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-120552 |
|
|
Homo sapiens |
|
pmid |
sentence |
14699954 |
The targets of jnk include the transcription factors p53. P75ntr-mediated apoptosis was shown to be dependent of p53 |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
RNF38 | down-regulates activity
ubiquitination
|
TP53 |
0.371 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-272130 |
|
|
Homo sapiens |
HEK-293 Cell |
pmid |
sentence |
23973461 |
Here we demonstrate that RNF38 is a functional ubiquitin protein ligase (E3). We show that RNF38 isoform 1 is localized to the nucleus by a bipartite nuclear localization sequence (NLS). We confirm that RNF38 is a binding partner of p53 and demonstrate that RNF38 can ubiquitinate p53 in vitro and in vivo. Finally, we show that overexpression of RNF38 in HEK293T cells results in relocalization of p53 to discrete foci associated with PML nuclear bodies. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
BBC3 |
0.683 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-140245 |
|
|
Homo sapiens |
HCT-116 Cell |
pmid |
sentence |
16151013 |
Nuclear p53 caused expression of puma, which then displaced p53 from bcl-xl, allowing p53 to induce mitochondrial permeabilization. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Mitochondrial Control of Apoptosis |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
FASLG |
0.415 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-62379 |
|
|
Homo sapiens |
|
pmid |
sentence |
9841917 |
Cd95l, cd95, and the trail death receptors are induced by the tumour suppressor p53 |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Mitochondrial Control of Apoptosis |
+ |
RFWD3 | up-regulates quantity by stabilization
ubiquitination
|
TP53 |
0.368 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-271944 |
|
|
Homo sapiens |
NCI-H1299 Cell |
pmid |
sentence |
20173098 |
RFWD3 is a positive regulator of p53 abundance and regulates the G1 checkpoint in response to IR. We found that an E3 ubiquitin ligase RFWD3 (RNF201/FLJ10520) forms a complex with Mdm2 and p53 to synergistically ubiquitinate p53 and is required to stabilize p53 in the late response to DNA damage. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
BAX |
0.743 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-47541 |
|
|
Homo sapiens |
|
pmid |
sentence |
9122197 |
P53 can transcriptionally activate bax, a bcl-2 family member that promotes apoptosis |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, FLT3-ITD signaling, Mitochondrial Control of Apoptosis, Malignant Melanoma, p53 in cancer |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
OGG1 |
0.441 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255440 |
|
|
Homo sapiens |
|
pmid |
sentence |
16293709 |
Using gel-shift assays, we showed that p53 binds to its putative cis-elements within the hOGG1 promoter. In addition we demonstrated that supplementing p53 in HCT116p53-/- cells enhanced the transcription of hOGG1. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | down-regulates quantity by repression
transcriptional regulation
|
LRBA |
0.278 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-253847 |
|
|
Homo sapiens |
|
pmid |
sentence |
15064745 |
We also show that LRBA promoter activity and endogenous LRBA mRNA levels are reduced by p53 and increased by E2F1, indicating that mutations in the tumor suppressors p53 and Rb could contribute to the deregulation of LRBA. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | down-regulates quantity by repression
transcriptional regulation
|
ABCB1 |
0.601 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255435 |
|
|
Homo sapiens |
|
pmid |
sentence |
10029407 |
p53 transcriptionally activates expression of the genes encoding epidermal growth factor receptor, matrix metalloproteinase (MMP)-2, cathepsin D, and thrombospondin-1 but represses expression of the genes encoding basic fibroblast growth factor and multidrug resistance-1. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CD79B | up-regulates
|
TP53 |
0.313 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-93526 |
|
|
Homo sapiens |
B-lymphocyte |
pmid |
sentence |
12324477 |
Bcr ligation resulted in p53 activation including its phosphorylation at ser15 |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
PERP |
0.626 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-75877 |
|
|
Homo sapiens |
|
pmid |
sentence |
10733530 |
Perp induction is linked to p53-dependent apoptosis, including in response to e2f-1-driven hyperproliferation. Furthermore, analysis of the perp promoter suggests that perp is directly activated by p53. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
SIN3B | down-regulates activity
binding
|
TP53 |
0.511 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-266776 |
|
|
Homo sapiens |
HCT-116 Cell |
pmid |
sentence |
26181367 |
The present study shows that under bleomycin-induced stress, expression of Sin3B gets up-regulated and it gets recruited by p53 at its target promoters. Knockdown of Sin3B leads to impaired negative regulation of p53 target genes and thus exemplifies Sin3B as a critical player in down-regulation of p53 subset target genes. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | down-regulates quantity by repression
transcriptional regulation
|
BIRC5 |
0.544 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-117328 |
|
|
Homo sapiens |
|
pmid |
sentence |
11965534 |
Further analyses suggested that the modification of chromatin within the survivin promoter could be a molecular explanation for silencing of survivin gene transcription by p53. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | down-regulates activity
binding
|
G6PD |
0.57 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-267468 |
|
|
Homo sapiens |
U2-OS Cell, HCT-116 Cell |
pmid |
sentence |
21336310 |
The p53 protein binds to glucose-6-phosphate dehydrogenase (G6PD), the first and rate-limiting enzyme of the PPP, and prevents the formation of the active dimer. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Pentose phosphate pathway |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
MDM2 |
0.968 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-34962 |
|
|
Mus musculus |
|
pmid |
sentence |
7958853 |
The p53 tumor suppressor protein trans-activates mdm2 itself, which is therefore considered a component of a p53 negative feedback loop. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, DNMT3A in AML, IDH-TET in AML, miRNA in AML, NPM1 in AML, FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, Luminal Breast Cancer, Malignant Melanoma, Triple mutant AML, NPM1_new, Prostate Cancer, p53 in cancer, Pancreatic ductal adenocarcinoma (PDA) |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
MMP2 |
0.458 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255432 |
|
|
Homo sapiens |
|
pmid |
sentence |
10029407 |
p53 transcriptionally activates expression of the genes encoding epidermal growth factor receptor, matrix metalloproteinase (MMP)-2, cathepsin D, and thrombospondin-1 but represses expression of the genes encoding basic fibroblast growth factor and multidrug resistance-1. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
AIFM1 |
0.359 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-267462 |
|
|
Homo sapiens |
|
pmid |
sentence |
23506862 |
P53 regulates basal expression of AIF and SCO2 and facilitates oxidative phosphorylation. The expression of GLUT1, GLUT4, and HK2 is negatively regulated by p53, whereas TIGAR expression is induced by p53. The net result of p53-mediated regulation of these glycolytic enzymes is the suppression of glycolysis. In addition, p53 directly binds and inhibits G6PD activity and downregulates the pentose phosphate pathway. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
USP7 | up-regulates
deubiquitination
|
TP53 |
0.731 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-139456 |
|
|
Homo sapiens |
|
pmid |
sentence |
16082221 |
Hausp counteracts the destabilizing effect of mdm2 by direct deubiquitination of p53. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | EBV infection |
+ |
Cullin 1-RBX1-Skp1 | down-regulates quantity by destabilization
ubiquitination
|
TP53 |
0.397 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-273449 |
|
|
Homo sapiens |
HCA-7 Cell |
pmid |
sentence |
26868148 |
We demonstrate here that SCFFbxo22-KDM4A is a senescence-associated E3 ligase targeting methylated p53 for degradation. We find that Fbxo22 is highly expressed in senescent cells in a p53-dependent manner, and that SCFFbxo22 ubiquitylated p53 and formed a complex with a lysine demethylase, KDM4A. |SCFFbxo22 forms a ternary complex with p53 and KDM4A that targets methylated p53 for degradation. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
EP300 | up-regulates activity
acetylation
|
TP53 |
0.909 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-261496 |
|
|
Homo sapiens |
|
pmid |
sentence |
25545885 |
C-terminal acetylation of p53 by p300/CBP and PCAF promotes an open conformation of p53 by preventing the occlusion of the DNA binding domain by the C-terminal tail. This enhances p53 transcriptional activity, leading to growth arrest and/or apoptosis |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, p53 in cancer |
+ |
DRAM2 | down-regulates quantity by repression
transcriptional regulation
|
TP53 |
0.312 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-259146 |
|
|
Homo sapiens |
|
pmid |
sentence |
30755245 |
DRAM2 plays an oncogenic role in NSCLC via regulating p53 expression. Knockdown of DRAM2 caused an increase of p53 and p21 expression, and overexpression of p53 caused a decrease of DRAM2 expression. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates activity
binding
|
PHB |
0.455 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-268978 |
|
|
|
|
pmid |
sentence |
16918502 |
Our previous studies have shown that prohibitin physically interacts with the marked-box domain of E2F family members and represses their transcriptional activity; in contrast, prohibitin could bind to and enhance the transcriptional activity of p53. |
|
Publications: |
1 |
+ |
SPRY4 | up-regulates quantity by expression
transcriptional regulation
|
TP53 |
0.271 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-253040 |
|
|
Homo sapiens |
Non-small Cell Lung Cancer Cell |
pmid |
sentence |
20501643 |
When Spry4 was stably transfected into H157 and H2122 NSCLC cell lines, decreased migration and invasion were observed. Matrix metalloproteinase-9 activity was decreased, and the expression of matrix metalloproteinase inhibitors TIMP1 and CD82 were increased. Stable expression of Spry4 led to reduced cell growth and reduced anchorage-independent growth in NSCLC cell lines, along with upregulation of tumor suppressors p53 and p21. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
4-(2,6-dichlorobenzamido)-N-(piperidin-4-yl)-pyrazole-3-carboxamide | down-regulates
chemical inhibition
|
TP53 |
0.8 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-189999 |
|
|
Homo sapiens |
|
pmid |
sentence |
Other |
|
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MSL2 | down-regulates activity
ubiquitination
|
TP53 |
0.378 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-271774 |
|
|
Homo sapiens |
NCI-H1299 Cell |
pmid |
sentence |
19033443 |
Here we describe MSL2, a novel E3 ligase for p53 that promotes ubiquitin-dependent cytoplasmic p53 localization. Unlike Mdm2 or most other p53 E3 ligases, MSL2-mediated p53 ubiquitination does not affect the stability of p53. Moreover, the MSL2-mediated effect on p53 is Mdm2-independent. Thus, our study identifies an important ubiquitin-ligase for modulating p53 subcellular localization. MSL2 ubiquitination of p53 is required for p53 cytoplasmic localization. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CDKN2A | up-regulates quantity by stabilization
|
TP53 |
0.78 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255694 |
|
|
Homo sapiens |
|
pmid |
sentence |
12091906 |
P14/p19 ARF functions by antagonizing MDM2 and thereby stabilizing p53 (refs. 17,18). Thus, loss of p14/p19ARF impairs p53-mediated growth arrest and/or apoptosis in response to activated oncogenes |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, DNMT3A in AML, Onco-fusion proteins in AML, NPM1 in AML, AML_TRIPLETS, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, Malignant Melanoma, Triple mutant AML, NPM1_new |
+ |
DNA_damage | up-regulates quantity
|
TP53 |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-209690 |
|
|
Homo sapiens |
|
pmid |
sentence |
19879762 |
In the case of DNA-damage, phosphorylation of both p53 and Mdm2 by the checkpoint kinases ATM, ATR, Chk1 and Chk2 contributes to the dissociation of the Mdm2-p53 complex, leading to enhanced cellular p53 levels that primarily accumulate in the nucleus. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Colorectal Carcinoma, FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, Mitochondrial Control of Apoptosis, Non-small-cell lung cancer (NSCLC), P38 Signaling, p53 in cancer |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
SIAH1 |
0.381 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-122986 |
|
|
Homo sapiens |
|
pmid |
sentence |
14985507 |
Northern blot analysis with a specific probe demonstrates an increase in siah-1b transcription on activation of endogenous and inducible exogenous p53. To explore whether this effect is directly mediated by p53 we analyzed 20 kb of chromosome x dna, containing the siah-1b locus. A p53-binding site was identified in the siah-1b promoter, located at nucleotides -2155/-2103 relative to the translational start site. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-271953 |
|
|
Homo sapiens |
HEK-293 Cell |
pmid |
sentence |
20181957 |
P53 directly induces the expression of Siah-1 and in turn formation of a unique SCF-like complex (SCF(TBL1)) comprised of Siah-1, Siah-1-interacting protein (SIP), Skp1, transducin β-like 1 (TBL1), and APC |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
THBS1 |
0.453 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255433 |
|
|
Homo sapiens |
|
pmid |
sentence |
10029407 |
p53 transcriptionally activates expression of the genes encoding epidermal growth factor receptor, matrix metalloproteinase (MMP)-2, cathepsin D, and thrombospondin-1 but represses expression of the genes encoding basic fibroblast growth factor and multidrug resistance-1. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
KLF4 | down-regulates quantity by repression
transcriptional regulation
|
TP53 |
0.577 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-270544 |
|
|
|
|
pmid |
sentence |
17308127 |
Previous work has shown that the Kruppel-like factor 4 (KLF4) transcription factor represses p53 transcription by binding to the PE21 element. |
|
Publications: |
1 |
+ |
TRIM24 | down-regulates
ubiquitination
|
TP53 |
0.547 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-188726 |
|
|
Homo sapiens |
|
pmid |
sentence |
19844164 |
New ring-domain e3-ubiquitin ligase trim24 that targets p53 for degradation |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | down-regulates quantity by repression
transcriptional regulation
|
Hexokinase |
0.423 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-270272 |
|
|
Homo sapiens |
|
pmid |
sentence |
27692180 |
P53 regulates basal expression of AIF and SCO2 and facilitates oxidative phosphorylation. The expression of GLUT1, GLUT4, and HK2 is negatively regulated by p53, whereas TIGAR expression is induced by p53. The net result of p53-mediated regulation of these glycolytic enzymes is the suppression of glycolysis. In addition, p53 directly binds and inhibits G6PD activity and downregulates the pentose phosphate pathway. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Glycolysis and Gluconeogenesis |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
CDKN1A |
0.873 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-254484 |
|
|
Homo sapiens |
|
pmid |
sentence |
14522900 |
In this study, we found that a subset of ING family members strongly repressed human alpha-fetoprotein (AFP) promoter activity but stimulated the p21(WAF1) promoter in parallel experiments in the same cell type, similar to the effects of p53. Both ING1 and p53 were able to suppress AFP transcription and cause p21 induction |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML, FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer |
+ |
CBFbeta-MYH11 | down-regulates quantity by repression
transcriptional regulation
|
TP53 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-256132 |
|
|
Mus musculus |
|
pmid |
sentence |
9834241 |
CBFbeta-SMMHC, Expressed in M4eo Acute Myeloid Leukemia, Reduces p53 Induction and Slows Apoptosis in Hematopoietic Cells Exposed to DNA-damaging Agents Reduced p53 induction may be caused in part by direct inhibition of p53 gene transcription, because p53 mRNA levels were reduced by CBFβ-SMMHC. Attenuated p53 induction and slowed apoptosis may contribute to leukemogenesis by CBFβ-SMMHC. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
Pathways: | Acute Myeloid Leukemia, Onco-fusion proteins in AML, KIT in AML |
+ |
Nutlin-3 | up-regulates
|
TP53 |
0.8 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255471 |
|
|
Homo sapiens |
|
pmid |
sentence |
17700533 |
Nutlin, a class of small molecule antagonist of HDM2, binds to the p53-binding pocket of HDM2, preventing p53 from binding to HDM2 and thus, resulting in stabilization and activation of p53 |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
CCNG1 |
0.782 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-268960 |
|
|
|
|
pmid |
sentence |
7957050 |
Using a DNA binding assay, a specific p53 binding site was identified upstream from the cyclin G gene, which functioned as a p53-dependent cis-acting element in a transient transfection assay. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-268961 |
|
|
Rattus norvegicus |
|
pmid |
sentence |
9688532 |
Individual promoter and intron p53-binding motifs from the rat Cyclin G1 promoter region support transcriptional activation by p53 but do not show co-operative activation. |
|
Publications: |
2 |
Organism: |
, Rattus Norvegicus |
+ |
TP53BP2 | up-regulates
binding
|
TP53 |
0.895 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-114762 |
|
|
Homo sapiens |
|
pmid |
sentence |
11839776 |
53bp2 interacts with the tumour suppressor p53 and enhances p53-mediated activation of transcription, possibly by facilitating the dephosphorylation of one or more sites on p53 |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
ZDHHC5 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-261150 |
|
|
Homo sapiens |
|
pmid |
sentence |
28775165 |
Mechanistic investigations revealed that mutant p53 transcriptionally upregulated ZDHHC5 along with the nuclear transcription factor NF-Y |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
DDX5 | up-regulates
binding
|
TP53 |
0.69 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-133341 |
|
|
Homo sapiens |
|
pmid |
sentence |
15660129 |
The dead box protein p68: a novel transcriptional coactivator of the p53 tumour suppressor |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
ARMC10 | down-regulates activity
binding
|
TP53 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-266414 |
|
|
Homo sapiens |
SAOS-2 Cell, BEL-7404 Cell |
pmid |
sentence |
17904127 |
Co-immunoprecipitation and GST pull-down assays have demonstrated that SVH-B directly interacts with p53. In both BEL-7404 cells and p53-null Saos-2 cells transfected with a temperature-sensitive mutant of p53, V143A, ectopically expressed SVH-B suppresses the transcriptional activity of p53, and suppression of SVH by RNA interference increases the transcriptional activity of p53. Our results suggested the function of SVH-B in accelerating growth and inhibition of apoptosis is related to its inhibitory binding to p53. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MAPK11 | up-regulates
phosphorylation
|
TP53 |
0.594 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-152843 |
|
|
Homo sapiens |
|
pmid |
sentence |
17254968 |
We show that prak activates p53 by direct phosphorylation. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
NKX3-1 | up-regulates quantity by stabilization
|
TP53 |
0.364 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251548 |
|
|
Homo sapiens |
|
pmid |
sentence |
16697957 |
NKX3.1 stabilizes p53.NKX3.1 can physically associate with HDAC1 and promotes p53 acetylation by recruiting HDAC1 from p53-MDM2-HDAC1 complex |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Prostate Cancer |
+ |
TP53 | down-regulates
|
Glycolysis |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-267467 |
|
|
Homo sapiens |
|
pmid |
sentence |
27692180 |
P53 regulates basal expression of AIF and SCO2 and facilitates oxidative phosphorylation. The expression of GLUT1, GLUT4, and HK2 is negatively regulated by p53, whereas TIGAR expression is induced by p53. The net result of p53-mediated regulation of these glycolytic enzymes is the suppression of glycolysis. In addition, p53 directly binds and inhibits G6PD activity and downregulates the pentose phosphate pathway. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
VCAN |
0.295 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255441 |
|
|
Homo sapiens |
|
pmid |
sentence |
12438652 |
By using in vitro and in vivo assays, we showed CSPG2 to be directly transactivated by p53. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
NOXA1 |
0.263 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-209687 |
|
|
Homo sapiens |
|
pmid |
sentence |
19879762 |
As a transcription factor, p53 induces several pro-apoptotic Bcl-2 members including Bax, Puma, Noxa and Bid, and represses the transcription of certain anti-apoptotic genes, including those encoding Bcl-2, Bcl-xL and survivin 3_and_5. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Mitochondrial Control of Apoptosis |
+ |
PLK1 | down-regulates
|
TP53 |
0.594 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-185841 |
|
|
Homo sapiens |
|
pmid |
sentence |
19473992 |
Plk1-mediated phosphorylation of topors regulates p53 stability. Herein, we have identified topoisomerase i-binding protein (topors), a p53-binding protein, as a plk1 target. We show that plk1 phosphorylates topors on ser(718) in vivo. Significantly, expression of a plk1-unphosphorylatable topors mutant (s718a) leads to a dramatic accumulation of p53 through inhibition of p53 degradation. Topors is an ubiquitin and small ubiquitin-like modifier ubiquitin-protein isopeptide ligase (sumo e3) ligase. Plk1-mediated phosphorylation of topors inhibits topors-mediated sumoylation of p53, whereas p53 ubiquitination is enhanced, leading to p53 degradation. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
JNK | up-regulates
phosphorylation
|
TP53 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-269985 |
|
|
Homo sapiens |
|
pmid |
sentence |
14699954 |
The targets of jnk include the transcription factors p53. P75ntr-mediated apoptosis was shown to be dependent of p53 |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | EBV infection, FLT3-ITD signaling |
+ |
OTUB1 | up-regulates quantity by stabilization
deubiquitination
|
TP53 |
0.546 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-276528 |
|
|
|
|
pmid |
sentence |
34785775 |
Furthermore, although OTUB1 dramatically induced p53 deubiquitination, its mutant (S16A) and deletion mutant did not have this effec |
|
Publications: |
1 |
+ |
MDM4 | down-regulates quantity by destabilization
ubiquitination
|
TP53 |
0.947 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-271389 |
|
|
in vitro |
|
pmid |
sentence |
12393902 |
Here we demonstrate that MdmX acts as a ubiquitin ligase in vitro, being capable of autoubiquitination, as well as mediating the ubiquitination of p53. |
|
Publications: |
1 |
Organism: |
In Vitro |
+ |
TP53 | down-regulates quantity by repression
transcriptional regulation
|
GMPS |
0.387 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-267342 |
|
|
Homo sapiens |
Hep-G2 Cell, SK-HEP-1 Cell, HuH-6 Cell |
pmid |
sentence |
27939741 |
Herein, we identified GMP synthetase (GMPS), a key enzyme of de novo purine biosynthesis, as an important p53 repression target using a large-scale proteomics approach. This p53-mediated repression of GMPS could be validated by immunoblotting in Sk-Hep1, HepG2, and HuH6 cells. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
HDAC8 | down-regulates activity
deacetylation
|
TP53 |
0.468 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255738 |
|
|
Mus musculus |
32D Cell |
pmid |
sentence |
26387755 |
HDAC8 mediates CM-induced deacetylation of p53.Collectively, these results indicate that although binding to p53 and HDAC8 occurs through distinct regions of the CM protein, simultaneous interaction with HDAC8 and p53 is required for aberrant deacetylation and inactivation of p53. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
GLS2 |
0.617 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-268041 |
|
|
Homo sapiens |
|
pmid |
sentence |
22307140 |
Glutaminase 2 (GLS2) can be directly transactivated by p53 and can therefore mediate p53-dependent regulation of cellular energy metabolism. G |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | down-regulates quantity by repression
transcriptional regulation
|
SLC2A1 |
0.584 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-267464 |
|
|
Homo sapiens |
|
pmid |
sentence |
27692180 |
P53 regulates basal expression of AIF and SCO2 and facilitates oxidative phosphorylation. The expression of GLUT1, GLUT4, and HK2 is negatively regulated by p53, whereas TIGAR expression is induced by p53. The net result of p53-mediated regulation of these glycolytic enzymes is the suppression of glycolysis. In addition, p53 directly binds and inhibits G6PD activity and downregulates the pentose phosphate pathway. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Glycolysis and Gluconeogenesis |
+ |
TP53 | up-regulates
|
CYCS |
0.469 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-140251 |
|
|
Homo sapiens |
|
pmid |
sentence |
19007744 |
P53 translocation precedes changes of mitochondrial membrane potential, cytochrome c release and caspase activation |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Mitochondrial Control of Apoptosis |
+ |
TP53 | up-regulates
binding
|
BAK1 |
0.678 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-124122 |
|
|
Homo sapiens |
|
pmid |
sentence |
15077116 |
P53 interacts with the pro-apoptotic mitochondrial membrane protein bak |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, Malignant Melanoma, Non-small-cell lung cancer (NSCLC) |
+ |
XPO1 | down-regulates activity
relocalization
|
TP53 |
0.566 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-260067 |
|
|
Homo sapiens |
|
pmid |
sentence |
17891139 |
We identify the major poly(ADP-ribosyl)ated sites of p53 by PARP-1 and find that PARP-1-mediated poly(ADP-ribosyl)ation blocks the interaction between p53 and the nuclear export receptor Crm1, resulting in nuclear accumulation of p53. These findings molecularly link PARP-1 and p53 in the DNA-damage response, providing the mechanism for how p53 accumulates in the nucleus in response to DNA damage.|PARP-1 is super-activated by binding to damaged DNA, and poly(ADP-ribosyl)ates p53. Poly(ADP-ribosyl)ation probably induces a structural change that mask the NES, and thus Crm1 can no longer target p53 to the nuclear export machinery, resulting in accumulation of p53 in the nucleus. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | FLT3-ITD signaling |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
TIGAR |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-267365 |
|
|
Homo sapiens |
T-47D Cell |
pmid |
sentence |
27803158 |
TP53 inducible glycolysis and apoptosis regulator (TIGAR) is a bisphosphatase that reduces glycolysis and is highly expressed in carcinoma cells in the majority of human breast cancers. TIGAR is the only known phosphatase glycolytic modulator regulated by TP53. The current study delineates the role of TIGAR in OXPHOS and glycolytic metabolic reprogramming in breast cancer. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
FBXO22 | down-regulates quantity by destabilization
ubiquitination
|
TP53 |
0.346 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-273448 |
|
|
Homo sapiens |
HCA-7 Cell |
pmid |
sentence |
26868148 |
We demonstrate here that SCFFbxo22-KDM4A is a senescence-associated E3 ligase targeting methylated p53 for degradation. We find that Fbxo22 is highly expressed in senescent cells in a p53-dependent manner, and that SCFFbxo22 ubiquitylated p53 and formed a complex with a lysine demethylase, KDM4A. |SCFFbxo22 forms a ternary complex with p53 and KDM4A that targets methylated p53 for degradation. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TOPORS | down-regulates
ubiquitination
|
TP53 |
0.473 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-185848 |
|
|
Homo sapiens |
|
pmid |
sentence |
19473992 |
Plk1-mediated phosphorylation of topors regulates p53 stabilityherein, we have identified topoisomerase i-binding protein (topors), a p53-binding protein, as a plk1 target. We show that plk1 phosphorylates topors on ser(718) in vivo. Significantly, expression of a plk1-unphosphorylatable topors mutant (s718a) leads to a dramatic accumulation of p53 through inhibition of p53 degradation. Topors is an ubiquitin and small ubiquitin-like modifier ubiquitin-protein isopeptide ligase (sumo e3) ligase. Plk1-mediated phosphorylation of topors inhibits topors-mediated sumoylation of p53, whereas p53 ubiquitination is enhanced, leading to p53 degradation. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | down-regulates quantity by repression
transcriptional regulation
|
TBXAS1 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-254086 |
|
|
Homo sapiens |
|
pmid |
sentence |
14586398 |
We demonstrate that p53 and ets-1 coregulate TXSA in an antagonistic and inter-related manner, with ets-1 being a potent transcriptional activator and p53 inhibiting ets-1-dependent transcription. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
AIFM2 |
0.482 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-261808 |
|
|
Homo sapiens |
|
pmid |
sentence |
12135761 |
The p53 tumor suppressor protein induces cell cycle arrest or apoptosis in response to cellular stresses. We have identified PRG3 (p53-responsive gene 3), which is induced specifically under p53-dependent apoptotic conditions in human colon cancer cells, and encodes a novel polypeptide of 373 amino acids with a predicted molecular mass of 40.5 kDa. these results support the hypothesis that the expression of the PRG3 gene in cells undergoing p53‐dependent apoptosis involves direct activation of its promoter by p53. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
NUMB | up-regulates
binding
|
TP53 |
0.531 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-178668 |
|
|
Homo sapiens |
Breast Cancer Cell |
pmid |
sentence |
18492217 |
Numb can actually interact in vivo with endogenous mdm2 and p53, resulting in a trimeric complex between the three proteins [10]. This interaction appears to regulate the stability of p53, as reduction of numb levels by rna interference (rnai) causes a decrease in the half-life of p53 and consequently a reduction in steady-state levels of the protein. Consistent with this observation, overexpression of numb increases the level of p53 in both unstressed and stressed cells. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates
binding
|
NFKB2 |
0.436 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-149811 |
|
|
Homo sapiens |
|
pmid |
sentence |
16990795 |
P52 cooperates with p53 to regulate other known p53 target genes. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
CTSD |
0.372 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255434 |
|
|
Homo sapiens |
|
pmid |
sentence |
10029407 |
p53 transcriptionally activates expression of the genes encoding epidermal growth factor receptor, matrix metalloproteinase (MMP)-2, cathepsin D, and thrombospondin-1 but represses expression of the genes encoding basic fibroblast growth factor and multidrug resistance-1. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates quantity
transcriptional regulation
|
MLH1 |
0.595 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-257605 |
|
|
Homo sapiens |
|
pmid |
sentence |
15781865 |
.... numerous potentially novel targets, including the DNA mismatch repair genes MLH1 and PMS2. Both of these genes were determined to be responsive to DNA damage and p53 activation in normal human fibroblasts, and have p53-response elements within their first intron. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CBFbeta-MYH11 | down-regulates activity
binding
|
TP53 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255737 |
|
|
Mus musculus |
32D Cell |
pmid |
sentence |
26387755 |
Here, we show that p53 activity is inhibited in inv(16)+ AML LSCs via interactions with the CBFβ-SMMHC (CM) fusion protein and histone deacetylase 8 (HDAC8).Altogether, these results indicate that CM fusion protein binds to p53 and impairs acetylation and activation of p53. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
Pathways: | Acute Myeloid Leukemia, Onco-fusion proteins in AML, KIT in AML |
+ |
ING1 | up-regulates quantity by expression
transcriptional regulation
|
TP53 |
0.494 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-254490 |
|
|
Homo sapiens |
U2-OS Cell |
pmid |
sentence |
15662138 |
Ectopic expression of p33ING1b could obviously upregulate p53, p21WAF1 and bax protein levels and activate caspase-3 in taxol-treated U2OS cells. Taken together, our data demonstrate that p33ING1b enhances taxol-induced apoptosis through p53-dependent pathway in human osteosarcoma cells. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
SCO2 |
0.625 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-267463 |
|
|
Homo sapiens |
|
pmid |
sentence |
27692180 |
P53 regulates basal expression of AIF and SCO2 and facilitates oxidative phosphorylation. The expression of GLUT1, GLUT4, and HK2 is negatively regulated by p53, whereas TIGAR expression is induced by p53. The net result of p53-mediated regulation of these glycolytic enzymes is the suppression of glycolysis. In addition, p53 directly binds and inhibits G6PD activity and downregulates the pentose phosphate pathway. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MDGA2 | up-regulates quantity by expression
transcriptional regulation
|
TP53 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-264241 |
|
|
Homo sapiens |
|
pmid |
sentence |
26206665 |
Enhanced protein expression of p53 and p21 by MDGA2 was confirmed in MDGA2 overexpressed cells and xenograft tumours. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
U2AF1 | down-regulates quantity by repression
transcriptional regulation
|
TP53 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-261512 |
|
|
Homo sapiens |
|
pmid |
sentence |
31144421 |
Our results further showed that knockdown of U2AF1 significantly Western blot analysis revealed an increase in the protein levels of downstream targets of p53 following U2AF1 knockdown. The data further showed that depletion of U2AF1 altered alternatively spliced apoptosis-associated gene transcripts in CFU-E cells. Our findings elucidate the role of U2AF1 in human erythropoiesis and reveal the underlying mechanisms. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TP53 | down-regulates quantity by repression
transcriptional regulation
|
DRAM2 |
0.312 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-259148 |
|
|
Homo sapiens |
|
pmid |
sentence |
30755245 |
DRAM2 plays an oncogenic role in NSCLC via regulating p53 expression. Knockdown of DRAM2 caused an increase of p53 and p21 expression, and overexpression of p53 caused a decrease of DRAM2 expression. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |