+ |
GSK3B | down-regulates quantity by destabilization
phosphorylation
|
CDKN1A |
0.411 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-152941 |
Ser114 |
EEDHVDLsLSCTLVP |
Homo sapiens |
MCF-7 Cell |
pmid |
sentence |
17283049 |
Glycogen synthase kinase 3beta phosphorylates p21waf1/cip1 for proteasomal degradation after uv irradiationhere, we show that ser-114 phosphorylation of p21 protein by glycogen synthase kinase 3beta (gsk-3beta) is required for its degradation in response to uv irradiation |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition |
+ |
CDK6 | down-regulates activity
phosphorylation
|
CDKN1A |
0.859 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-144832 |
Ser130 |
SGEQAEGsPGGPGDS |
Homo sapiens |
|
pmid |
sentence |
16508017 |
Here, we show that p21cip1 is associated with k cyclin both in overexpression models and in primary effusion lymphoma cells and is a substrate of the k cyclin/cdk6 complex, resulting in phosphorylation of p21cip1 on serine 130. This phosphoform of p21cip1 appeared unable to associate with cdk2 in vivo. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia |
+ |
CDK2 | down-regulates quantity by destabilization
phosphorylation
|
CDKN1A |
0.953 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-149416 |
Ser130 |
SGEQAEGsPGGPGDS |
Homo sapiens |
|
pmid |
sentence |
15964852 |
Cdk2 destabilizes p21 via the cy2 cyclin-binding motif and p21 phosphorylation at ser-130. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MAPK8 | up-regulates quantity by stabilization
phosphorylation
|
CDKN1A |
0.659 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-89440 |
Ser130 |
SGEQAEGsPGGPGDS |
Homo sapiens |
|
pmid |
sentence |
12058028 |
The stress-activated protein kinases p38 alpha and jnk1 stabilize p21(cip1) by phosphorylation.|p38 alpha and JNK1 phosphorylated p21 in vivo, and both p38 alpha and JNK1 phosphorylated p21 at Ser(130) in vitro. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-250118 |
Thr57 |
NFDFVTEtPLEGDFA |
in vitro |
|
pmid |
sentence |
12058028 |
P38α and JNK1 Phosphorylate p21 in Vitro at Thr57 and Ser130. These data suggest that phosphorylation at Thr57 is necessary for stabilization of p21. |
|
Publications: |
2 |
Organism: |
Homo Sapiens, In Vitro |
Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML |
+ |
MAPK1 | down-regulates quantity by destabilization
phosphorylation
|
CDKN1A |
0.373 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-185215 |
Ser130 |
SGEQAEGsPGGPGDS |
Homo sapiens |
|
pmid |
sentence |
19364816 |
Extracellular signal-regulated kinase 2-dependent phosphorylation induces cytoplasmic localization and degradation of p21cip1.|Phosphopeptide analysis of in vitro ERK2-phosphorylated p21(Cip1) revealed two phosphorylation sites, Thr57 and Ser130. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-185219 |
Thr57 |
NFDFVTEtPLEGDFA |
Homo sapiens |
|
pmid |
sentence |
19364816 |
We have shown that erk2 interacts with and phosphorylates p21cip1, promoting p21cip1_ubiquitination. We identified two erk2 phosphorylation sites, thr57 and ser130, in p21cip1_and showed that phosphorylation of these residues increases p21cip1_cytoplasmic distribution and proteasome-dependent degradation. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
MAPK14 | up-regulates quantity by stabilization
phosphorylation
|
CDKN1A |
0.457 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-89436 |
Ser130 |
SGEQAEGsPGGPGDS |
Homo sapiens |
|
pmid |
sentence |
12058028 |
The stress-activated protein kinases p38 alpha and jnk1 stabilize p21(cip1) by phosphorylation.|p38 alpha and JNK1 phosphorylated p21 in vivo, and both p38 alpha and JNK1 phosphorylated p21 at Ser(130) in vitro. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | FLT3-ITD signaling |
+ |
ERK1/2 | down-regulates quantity by destabilization
phosphorylation
|
CDKN1A |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-244618 |
Ser130 |
SGEQAEGsPGGPGDS |
Homo sapiens |
|
pmid |
sentence |
19364816 |
Extracellular signal-regulated kinase 2-dependent phosphorylation induces cytoplasmic localization and degradation of p21cip1.|Phosphopeptide analysis of in vitro ERK2-phosphorylated p21(Cip1) revealed two phosphorylation sites, Thr57 and Ser130. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-244513 |
Thr57 |
NFDFVTEtPLEGDFA |
Homo sapiens |
|
pmid |
sentence |
19364816 |
We have shown that erk2 interacts with and phosphorylates p21cip1, promoting p21cip1_ubiquitination. We identified two erk2 phosphorylation sites, thr57 and ser130, in p21cip1_and showed that phosphorylation of these residues increases p21cip1_cytoplasmic distribution and proteasome-dependent degradation. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML, FLT3-ITD signaling, Rhabdomyosarcoma |
+ |
STK38 | down-regulates quantity by destabilization
phosphorylation
|
CDKN1A |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-272961 |
Ser146 |
GRKRRQTsMTDFYHS |
Homo sapiens |
HEK-293 Cell |
pmid |
sentence |
21262772 |
More importantly, with the direct regulation of p21 stability by phosphorylation on Ser 146, we define here the first downstream signaling mechanisms by which NDR kinases can control G1/S progression.|NDR kinases regulate p21 stability by phosphorylation of S146 on p21. | |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
PLCG2 | up-regulates quantity by stabilization
phosphorylation
|
CDKN1A |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-262963 |
Ser146 |
GRKRRQTsMTDFYHS |
Homo sapiens |
|
pmid |
sentence |
31575057 |
Phosphorylation at Ser-146 by PKCδ increases p21 stability |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
AKT1 | up-regulates quantity by stabilization
phosphorylation
|
CDKN1A |
0.835 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-157790 |
Ser146 |
GRKRRQTsMTDFYHS |
Homo sapiens |
|
pmid |
sentence |
31575057 |
Pim-1, PKC, and Akt1 kinases phosphorylate Thr-145 and Ser-146 sites on p21 protein. Phosphorylation at Thr-145 promotes cytoplasmic translocation and stability of p21. Ser-146 phosphorylation mediated by Akt1 enhances p21 stabilization and promotes cell survival. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-149698 |
Thr145 |
QGRKRRQtSMTDFYH |
Homo sapiens |
|
pmid |
sentence |
16982699 |
Whereas akt1 phosphorylates p21, inducing its release from cdk2 and cytoplasmic localization as previously described for akt, akt2 binds p21 in the region spanning the t145 site of p21, thus competing with phosphorylation by akt1 and inducing its accumulation in the nucleus. These distinct roles of akt/pkb isoforms in modulating proliferation and p21 have important implications for the development of drugs aimed at inhibiting cancer cell proliferation.[...] We next investigated if phosphorylation of p21-t145 interfered with akt2 binding. As shown in fig. ?Fig.8e8e (right lane), phosphorylation of p21 on t145 effectively prevented akt2 interaction. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
Pathways: | FLT3-ITD signaling |
+ |
PIM1 | up-regulates quantity by stabilization
phosphorylation
|
CDKN1A |
0.494 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-262961 |
Ser146 |
GRKRRQTsMTDFYHS |
Homo sapiens |
|
pmid |
sentence |
31575057 |
Pim-1, PKC, and Akt1 kinases phosphorylate Thr-145 and Ser-146 sites on p21 protein. Phosphorylation at Thr-145 promotes cytoplasmic translocation and stability of p21. Ser-146 phosphorylation mediated by Akt1 enhances p21 stabilization and promotes cell survival. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-164642 |
Thr145 |
QGRKRRQtSMTDFYH |
Homo sapiens |
|
pmid |
sentence |
20307683 |
Pim-2 phosphorylation of p21(cip1/waf1) enhances its stability and inhibits cell proliferation in hct116 cellshere we demonstrate that like pim-1, pim-2 also phosphorylates the cell cycle inhibitor p21(cip1/waf1) (p21) on thr145 in vitro and in vivo |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML, FLT3-ITD signaling |
+ |
PLCG1 | up-regulates quantity by stabilization
phosphorylation
|
CDKN1A |
0.266 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-262962 |
Ser146 |
GRKRRQTsMTDFYHS |
Homo sapiens |
|
pmid |
sentence |
31575057 |
Phosphorylation at Ser-146 by PKCδ increases p21 stability |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
PRKCA | up-regulates activity
phosphorylation
|
CDKN1A |
0.385 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-139302 |
Ser153 |
SMTDFYHsKRRLIFS |
Homo sapiens |
|
pmid |
sentence |
16055744 |
Binding of calmodulin to the carboxy-terminal region of p21 induces nuclear accumulation via inhibition of protein kinase c-mediated phosphorylation of ser153| When phosphorylated at Ser153, p21 is located at the cytoplasm and disrupts stress fibers. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
DYRK1B | up-regulates activity
phosphorylation
|
CDKN1A |
0.261 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-235635 |
Ser153 |
SMTDFYHsKRRLIFS |
Mus musculus |
|
pmid |
sentence |
15851482 |
Mirk exerts its anti-apoptotic effects during muscle differentiation at least in part through effects on the cell cycle inhibitor and pro-survival molecule p21cip1. Overexpression and rna interference experiments demonstrated that mirk phosphorylates p21 within its nuclear localization domain at ser-153 causing a portion of the typically nuclear p21 to localize in the cytoplasm.Translocation to the cytoplasm enables p21 to block apoptosis through inhibitory interaction with pro-apoptotic molecules. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
+ |
MAP3K5 | up-regulates
phosphorylation
|
CDKN1A |
0.575 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-153440 |
Ser98 |
GGRRPGTsPALLQGT |
Homo sapiens |
|
pmid |
sentence |
17325029 |
P21cip1 is phosphorylated in vitro by both ask1 and jnk1 at s98. /phosphorylation of p21cip1 at s98, which in vivo appears to be regulated by ask1, may therefore mediate negative feedback in the ask1 signaling pathway. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
DAPK3 | up-regulates quantity by stabilization
phosphorylation
|
CDKN1A |
0.321 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251085 |
Thr145 |
QGRKRRQtSMTDFYH |
in vitro |
|
pmid |
sentence |
15001356 |
ZIP kinase phosphorylates p21(WAF1) at Thr145 and alanine-substituted mutations in the p21(WAF1) phosphorylation site alter its ability to be phosphorylated by ZIP kinase. | Transfected ZIPK can promote the phosphorylation of p21(WAF1) at Thr145 in vivo and can increase the half-life of p21(WAF1) |
|
Publications: |
1 |
Organism: |
In Vitro |
+ |
PIM | up-regulates quantity by stabilization
phosphorylation
|
CDKN1A |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-259424 |
Thr145 |
QGRKRRQtSMTDFYH |
Homo sapiens |
|
pmid |
sentence |
20307683 |
Pim-2 phosphorylation of p21(cip1/waf1) enhances its stability and inhibits cell proliferation in hct116 cellshere we demonstrate that like pim-1, pim-2 also phosphorylates the cell cycle inhibitor p21(cip1/waf1) (p21) on thr145 in vitro and in vivo |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML |
+ |
AKT | up-regulates quantity by stabilization
phosphorylation
|
CDKN1A |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-244180 |
Thr145 |
QGRKRRQtSMTDFYH |
Homo sapiens |
|
pmid |
sentence |
16982699 |
Whereas akt1 phosphorylates p21, inducing its release from cdk2 and cytoplasmic localization as previously described for akt, akt2 binds p21 in the region spanning the t145 site of p21, thus competing with phosphorylation by akt1 and inducing its accumulation in the nucleus. These distinct roles of akt/pkb isoforms in modulating proliferation and p21 have important implications for the development of drugs aimed at inhibiting cancer cell proliferation.[...] We next investigated if phosphorylation of p21-t145 interfered with akt2 binding. As shown in fig. ?Fig.8e8e (right lane), phosphorylation of p21 on t145 effectively prevented akt2 interaction. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-244184 |
Thr145 |
QGRKRRQtSMTDFYH |
Homo sapiens |
|
pmid |
sentence |
16982699 |
Whereas akt1 phosphorylates p21, inducing its release from cdk2 and cytoplasmic localization as previously described for akt. |
|
Publications: |
2 |
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, Rhabdomyosarcoma |
+ |
PIM2 | up-regulates quantity by stabilization
phosphorylation
|
CDKN1A |
0.413 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-164646 |
Thr145 |
QGRKRRQtSMTDFYH |
Homo sapiens |
|
pmid |
sentence |
20307683 |
Pim-2 phosphorylation of p21(cip1/waf1) enhances its stability and inhibits cell proliferation in hct116 cellsere we demonstrate that like pim-1, pim-2 also phosphorylates the cell cycle inhibitor p21(cip1/waf1) (p21) on thr145 in vitro and in vivo |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
PRKAA1 | down-regulates quantity by repression
transcriptional regulation
|
CDKN1A |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-186061 |
|
|
Homo sapiens |
Myoblast |
pmid |
sentence |
19491292 |
Activation of ampk reduced p21 protein and mrna expression, which was associated with re- duced g1/s cell cycle transition and p21 promoter activity. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Tissue: |
Muscle, Skeletal Muscle, Myotube |
+ |
TBX3 | down-regulates quantity by repression
transcriptional regulation
|
CDKN1A |
0.309 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-249602 |
|
|
Homo sapiens |
Rhabdomyosarcoma Cell Line |
pmid |
sentence |
25211658 |
TBX2 and TBX3 function as transcriptional repressors and both have been shown to inhibit myogenesis (Carlson et al, 2002; Zhu et al, 2014). Abnormal expression of TBX2 has been reported in several cancers including breast, pancreas, and melanoma, where it has been shown to drive proliferation (reviewed in Abrahams et al (2010)). As has been previously shown in other cell types, TBX2 was found to induce a downregulation of p14/19ARF and function as a direct repressor of p21 in RMS |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
SCF-SKP2 | down-regulates quantity by destabilization
ubiquitination
|
CDKN1A |
0.667 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-267556 |
|
|
Homo sapiens |
HaCaT Cell |
pmid |
sentence |
9736735 |
Human CUL-1 associates with the SKP1/SKP2 complex and regulates p21CIP1/WAF1 and cyclin D proteins|These data suggest that the human p19(SKP1)/p45(SKP2)/CUL-1 complex is likely to function as an E3 ligase to selectively target cyclin D and p21 for the ubiquitin-dependent protein degradation. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CDKN1A | down-regulates activity
binding
|
CyclinE/CDK2 |
0.887 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-245462 |
|
|
Homo sapiens |
MCF-7 Cell |
pmid |
sentence |
11154267 |
Overexpression of p16INK4a in cells with functional pRb results in inhibition of both Cdk4- and Cdk6-associated kinase activity and pRb phosphorylation, with subsequent cell cycle arrest (46, 50). In addition, inhibition of D cyclin-Cdk4 complex formation by p16INK4a prevents sequestration of p21Cip1 and p27Kip1 by these complexes in early G1, leading to suppression of cyclin E-Cdk2 activity |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer |
+ |
ESR2 | up-regulates quantity by expression
transcriptional regulation
|
CDKN1A |
0.295 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-253943 |
|
|
Homo sapiens |
Breast Cancer Cell Line |
pmid |
sentence |
11517191 |
ER beta and ER alpha induced the expression of several endogenous genes such as pS2, TGF alpha, or the cyclin kinase inhibitor p21 but, in contrast to ER alpha, ER beta was unable to regulate c-myc proto-oncogene expression |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MYOG | down-regulates quantity by repression
transcriptional regulation
|
CDKN1A |
0.338 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251575 |
|
|
Homo sapiens |
|
pmid |
sentence |
25211658 |
P21 is regulated by MyoD and myogenin in normal muscle cells and the inactivation of these factors in RMS cells contributes to the silencing of p21 in RMS cells |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Rhabdomyosarcoma |
+ |
ETV6 | up-regulates quantity by expression
transcriptional regulation
|
CDKN1A |
0.344 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-254138 |
|
|
Mus musculus |
32D Clone3 Cell |
pmid |
sentence |
16828711 |
Forced expression of TEL stimulated transcription via the p53-responsive element and increased the expression of cellular target genes for p53 such as cell cycle regulator p21 and apoptosis inducer Puma. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
Pathways: | Acute Myeloid Leukemia |
+ |
CDKN1A | down-regulates
binding
|
CDK4 |
0.939 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-29957 |
|
|
Homo sapiens |
|
pmid |
sentence |
7626805 |
P21cip1 is a cyclin-dependent kinase (cdk) inhibitor that is transcriptionally activated by p53 in response to dna damage.We Have explored the interaction of p21 with the currently known cdks. p21 effectively inhibits cdk2, cdk3, cdk4, and cdk6 kinases. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
LRRC4 | up-regulates quantity by expression
transcriptional regulation
|
CDKN1A |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-264055 |
|
|
Homo sapiens |
|
pmid |
sentence |
25526788 |
LRRC4/NGL-2 can delay the cell cycle in late G1 by increasing the expression of cell cycle inhibitory molecules (p21, p27) and reducing the expression of cell cycle regulatory proteins (CyclinD1, CDK2, CyclinE, CDK4) via the inhibition of K-Ras/c-Raf/ERK/MAPK, PI-3K/AKT/NF- κB, p70S6/PKC and STAT3, and the upregulation of the JNK2/c-Jun/mp53 signaling pathway. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Tissue: |
Brain |
+ |
CDKN1A | down-regulates activity
binding
|
CyclinB/CDK1 |
0.85 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251498 |
|
|
|
|
pmid |
sentence |
10913154 |
P21 Inhibits Thr161 Phosphorylation of Cdc2 to Enforce the G2 DNA Damage Checkpoint|The cyclin-dependent kinase inhibitor p21 is required for a sustained G2 arrest after activation of the DNA damage checkpoint. Here we have addressed the mechanism by which p21 can contribute to this arrest in G2. We show that p21 blocks the activating phosphorylation of Cdc2 on Thr161 |
|
Publications: |
1 |
Pathways: | Cell cycle: G2/M phase transition |
+ |
CELF6 | up-regulates quantity by stabilization
post transcriptional regulation
|
CDKN1A |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-269044 |
|
|
Homo sapiens |
HCT-116 Cell |
pmid |
sentence |
31534127 |
CELF6 binds to the 3'UTR of p21 transcript and increases its mRNA stability. Depletion of CELF6 promotes cell cycle progression, cell proliferation and colony formation whereas overexpression of CELF6 induces G1 phase arrest. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
KDM4B | down-regulates quantity by repression
transcriptional regulation
|
CDKN1A |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-263730 |
|
|
Homo sapiens |
HCT-116 Cell |
pmid |
sentence |
28073943 |
JMJD2B induction attenuates the transcription of key p53 transcriptional targets including p21, PIG3 and PUMA, and this modulation is dependent on the catalytic capacity of JMJD2B. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MYC | down-regulates quantity by repression
transcriptional regulation
|
CDKN1A |
0.772 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-102740 |
|
|
Homo sapiens |
|
pmid |
sentence |
12835716 |
C-myc also directly represses transcription of cdk kinase inhibitors including p27kip1, p21cip1, p15ink4b and p16ink4a |
|
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, Rhabdomyosarcoma |
+ |
CDKN1A | up-regulates
|
Cell_cycle_exit |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-241956 |
|
|
Mus musculus |
Myoblast |
pmid |
sentence |
9388774 |
The upregulation of the cyclin-dependent kinase inhibitor p21 and the dephosphorylation of retinoblastoma protein (pRb) appear to be critical regulatory events for the establishment ,,, the postmitotic ... states [in myoblasts differentiating into mature myotubes] |
|
Publications: |
1 |
Organism: |
Mus Musculus |
+ |
MDM2 | down-regulates quantity by destabilization
binding
|
CDKN1A |
0.664 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-272954 |
|
|
Homo sapiens |
PC-3 Cell |
pmid |
sentence |
14761977 |
MDM2 facilitates p21 degradation independent of ubiquitination and the E3 ligase function of MDM2. Instead, MDM2 promotes p21 degradation by facilitating binding of p21 with the proteasomal C8 subunit. The physical interaction between p21 and MDM2 was demonstrated both in vitro and in vivo with the binding region in amino acids 180-298 of the MDM2 protein. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer |
+ |
MKRN1 | down-regulates quantity by destabilization
polyubiquitination
|
CDKN1A |
0.318 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-271845 |
|
|
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. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
RNF126 | down-regulates quantity by destabilization
polyubiquitination
|
CDKN1A |
0.336 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-272033 |
|
|
Homo sapiens |
HEK-293 Cell |
pmid |
sentence |
23026136 |
E3 ubiquitin ligase RNF126 promotes cancer cell proliferation by targeting the tumor suppressor p21 for ubiquitin-mediated degradation.We showed that RNF126 interacts with p21 and RNF126 overexpression increased p21 protein ubiquitination in an E3 ligase activity-dependent manner. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
AKT | down-regulates activity
binding
|
CDKN1A |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-244187 |
|
|
Homo sapiens |
Myoblast |
pmid |
sentence |
16982699 |
More importantly, the consequences of phosphorylation of either Thr145 or Ser146 are distinct. When p21 is phosphorylated on Thr145, it localizes to the nucleus and results in the disruption of the association between proliferating cell nuclear antigen and p21. Furthermore, phosphorylation of Thr145 promotes stabilization of p21 |
|
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, Rhabdomyosarcoma |
+ |
MYC | down-regulates quantity by repression
transcriptional regulation
|
CDKN1A |
0.772 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-267574 |
|
|
Homo sapiens |
Lymphoma Cell |
pmid |
sentence |
20551174 |
In tissue culture, ectopic expression of Myc suppresses the cell cycle arrest that occurs in response to several anti-mitogenic signals such as transforming growth factor β (TGFβ), since Myc represses expression of the cyclin-dependent kinase inhibitors (CKIs) p15ink4b, p21cip1, and p57kip2 via interaction with Miz1 |
|
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, Rhabdomyosarcoma |
+ |
IMPDH2 | down-regulates quantity by repression
transcriptional regulation
|
CDKN1A |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-260959 |
|
|
Homo sapiens |
|
pmid |
sentence |
30518405 |
We further demonstrated that IMPDH2 overexpression accelerated G1/S phase cell cycle transition by inducing increased expression of cyclin D1 and Ki-67 and downregulation of p21Cip1 and p27Kip1. More importantly, G1/S phase cell cycle transition was triggered by IMPDH2 through activation of AKT activity, downregulation of mTOR and FOXO1 transcriptional activity. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
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 |
+ |
AKT2 | down-regulates activity
binding
|
CDKN1A |
0.669 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-149705 |
|
|
Homo sapiens |
Myoblast |
pmid |
sentence |
16982699 |
Whereas akt1 phosphorylates p21, inducing its release from cdk2 and cytoplasmic localization as previously described for akt, akt2 binds p21 in the region spanning the t145 site of p21, thus competing with phosphorylation by akt1 and inducing its accumulation in the nucleus. These distinct roles of akt/pkb isoforms in modulating proliferation and p21 have important implications for the development of drugs aimed at inhibiting cancer cell proliferation. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CDKN1A | down-regulates
binding
|
CDK2 |
0.953 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-149711 |
|
|
Homo sapiens |
Myoblast |
pmid |
sentence |
16982699 |
Considering that akt1 phosphorylates p21, this dissociation likely results from phosphorylation of p21 and release of cdk2. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MDM2 | down-regulates quantity by repression
|
CDKN1A |
0.664 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-160977 |
|
|
Homo sapiens |
|
pmid |
sentence |
18292944 |
Overexpression of hdm2 resulted in a decrease in the level of p21waf1 |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer |
+ |
RBM38 | up-regulates quantity by stabilization
post transcriptional regulation
|
CDKN1A |
0.325 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-275391 |
|
|
Homo sapiens |
|
pmid |
sentence |
17050675 |
Here, we found that RNPC1, an RNA-binding protein and a target of the p53 family, is required for maintaining the stability of the basal and stress-induced p21 transcript. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
KHSRP | down-regulates quantity by destabilization
post transcriptional regulation
|
CDKN1A |
0.255 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-235859 |
|
|
Mus musculus |
C2C12 Cell |
pmid |
sentence |
16364914 |
Importantly, KSRP knockdown in C2C12 GM cells (Figure 2D) stabilized endogenous my- ogenin and p21 transcripts (Figure 2E). Furthermore, stable knockdown of KSRP, using shRNA, induced the accumulation of p21 mRNA in C2C12 GM while it did not affect the expression of late myogenic markers (MHC and muscle-creatine kinase [MCK]) |
|
Publications: |
1 |
Organism: |
Mus Musculus |
+ |
POU5F1 | down-regulates quantity by repression
transcriptional regulation
|
CDKN1A |
0.413 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255043 |
|
|
Homo sapiens |
Embryonic Stem Cell |
pmid |
sentence |
19968627 |
p21 protein levels were repressed by Oct-4 and were induced by the down-regulation of Oct-4 in ZHBTc4 ES cells. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MYOD1 | up-regulates
transcriptional regulation
|
CDKN1A |
0.412 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251574 |
|
|
Homo sapiens |
|
pmid |
sentence |
25211658 |
P21 is regulated by MyoD and myogenin in normal muscle cells and the inactivation of these factors in RMS cells contributes to the silencing of p21 in RMS cells |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Rhabdomyosarcoma |
+ |
TCF3 | up-regulates quantity by expression
transcriptional regulation
|
CDKN1A |
0.321 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255385 |
|
|
Homo sapiens |
|
pmid |
sentence |
23684607 |
The transcription factor TCF3, also known as E2A, drives p21 expression while repressing PUMA across cancer cell types of multiple origins. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
RBPJ | up-regulates quantity by expression
transcriptional regulation
|
CDKN1A |
0.313 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-109042 |
|
|
Homo sapiens |
|
pmid |
sentence |
11432830 |
The rbp-jkappa protein binds directly to the endogenous p21 promoter and p21 expression is induced specifically by activated notch1 through rbp-jkappa-dependent transcription. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
STAT5A | up-regulates quantity by expression
transcriptional regulation
|
CDKN1A |
0.33 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-261518 |
|
|
Mus musculus |
|
pmid |
sentence |
15003515 |
Flt3 Mutation Activates p21WAF1/CIP1 Gene Expression Through the Action of STAT5. Co-transfection of p21 promoter-luciferase constructs with Flt3-ITD plasmid into K562 and BaF3 cells results in the induction of p21 promoter activity and a -692/-684 STAT site is important for the induction. STAT5a binds specifically to this element and Flt3-ITD enhances the protein binding to this site. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML, FLT3-ITD signaling |
+ |
ING1 | up-regulates quantity by expression
transcriptional regulation
|
CDKN1A |
0.313 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-254483 |
|
|
Homo sapiens |
Hep-G2 Cell |
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; hSIR2, a negative regulator of the p53 protein, showed the opposite effects on the AFP promoter and, like HDAC1, repressed p21 promoter activity. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
RNF144B | down-regulates quantity by destabilization
ubiquitination
|
CDKN1A |
0.366 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-271478 |
|
|
Homo sapiens |
HCT-116 Cell |
pmid |
sentence |
12853982 |
P53RFP, a p53-inducible RING-finger protein, regulates the stability of p21WAF1. Here we report the isolation of a novel transcriptional target of p53, designated p53RFP (p53-inducible RING-finger protein), whose product has E3 ubiquitin ligase activity. Its expression was negatively correlated to that of p21(WAF1) protein; p53RFP is likely to play a role in the regulation of this protein, probably through interaction with, and ubiquitination of, p21(WAF1). |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TBX2 | down-regulates quantity by repression
transcriptional regulation
|
CDKN1A |
0.353 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-249593 |
|
|
Homo sapiens |
Rhabdomyosarcoma Cell Line |
pmid |
sentence |
25211658 |
TBX2 and TBX3 function as transcriptional repressors and both have been shown to inhibit myogenesis (Carlson et al, 2002; Zhu et al, 2014). Abnormal expression of TBX2 has been reported in several cancers including breast, pancreas, and melanoma, where it has been shown to drive proliferation (reviewed in Abrahams et al (2010)). As has been previously shown in other cell types, TBX2 was found to induce a downregulation of p14/19ARF and function as a direct repressor of p21 in RMS |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Rhabdomyosarcoma |
+ |
CDKN1A | down-regulates
|
Cell_cycle_progress |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251564 |
|
|
Homo sapiens |
|
pmid |
sentence |
24470334 |
The cell cycle regulator p21 is induced early in myoblast differentiation and functions to block cell cycle progression |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
SPRY4 | up-regulates quantity by expression
transcriptional regulation
|
CDKN1A |
0.254 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-253041 |
|
|
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 |
+ |
NF90-NF45 | down-regulates quantity by repression
|
CDKN1A |
0.25 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-268491 |
|
|
Rattus norvegicus |
|
pmid |
sentence |
25566957 |
In the present study, we investigated the expression profiles of NF45 in the sciatic nerve of adult rats following crush injury. in the TNF-α-induced Schwann cell proliferation assay, protein level of NF45 and cyclin E was elevated while expression of p21 was down-regulated. Further, when NF45 was knocked down, Schwann cell proliferation was interrupted and the expression of cyclin E was attenuated, while the expression of p21 was up-regulated. To repress the expression of p21 is one of the basic mechanisms for NF45-regulated cell proliferation. |
|
Publications: |
1 |
Organism: |
Rattus Norvegicus |
+ |
CDKN1A | down-regulates
binding
|
PCNA |
0.754 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-191939 |
|
|
Homo sapiens |
|
pmid |
sentence |
22911014 |
P21 exerts its effect on the cell cycle not only by inhibiting cyclin/cdk complexes, but also by inhibiting proliferating cell nuclear antigen (pcna) |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CDKN1A | down-regulates
binding
|
CDK1 |
0.876 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-128442 |
|
|
Homo sapiens |
|
pmid |
sentence |
15340381 |
P21 and p27 are key inhibitors of both cdk1 and cdk2. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia |
+ |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
CDKN1A |
0.873 |
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. |
|
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. |
|
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 |
+ |
RBPJ/NOTCH | up-regulates quantity by expression
transcriptional regulation
|
CDKN1A |
0.346 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-252033 |
|
|
Mus musculus |
Keratinocyte |
pmid |
sentence |
15866158 |
Induction of the p21WAF1/Cip1 gene by Notch 1 activation in differentiating keratinocytes is associated with direct targeting of the RBP-J_ protein to the p21 promoter. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
+ |
CDKN1A | down-regulates
binding
|
CDK6 |
0.859 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-30030 |
|
|
Homo sapiens |
|
pmid |
sentence |
7626805 |
P21cip1 is a cyclin-dependent kinase (cdk) inhibitor that is transcriptionally activated by p53 in response to dna damage.We Have explored the interaction of p21 with the currently known cdks. p21 effectively inhibits cdk2, cdk3, cdk4, and cdk6 kinases |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia |
+ |
FUBP1 | up-regulates quantity by expression
transcriptional regulation
|
CDKN1A |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-259125 |
|
|
Homo sapiens |
|
pmid |
sentence |
19637194 |
In our analysis of FBP1 shRNA-transduced Hep3B cells, we found that p21 mRNA levels increase following FBP1 knockdown, suggesting that FBP1 functions as a repressor of p21. Our results identify the tumor suppressor p21 as the second direct FBP1 target gene in addition to the proto-oncogene c-myc. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
FLT3 | up-regulates quantity by expression
transcriptional regulation
|
CDKN1A |
0.293 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-261520 |
|
|
Mus musculus |
|
pmid |
sentence |
15003515 |
Flt3 Mutation Activates p21WAF1/CIP1 Gene Expression Through the Action of STAT5. Through the Action of STAT5. Co-transfection of p21 promoter-luciferase constructs with Flt3-ITD plasmid into K562 and BaF3 cells results in the induction of p21 promoter activity and a -692/-684 STAT site is important for the induction. STAT5a binds specifically to this element and Flt3-ITD enhances the protein binding to this site. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML, FLT3-ITD signaling |
+ |
CDKN1A | up-regulates activity
|
RB1 |
0.704 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-69925 |
|
|
Homo sapiens |
|
pmid |
sentence |
10439039 |
P21 may inhibit cell cycle progression by preventing the phosphorylation of prb. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer, Rhabdomyosarcoma |
+ |
SIRT2 | down-regulates quantity by repression
transcriptional regulation
|
CDKN1A |
0.315 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-254481 |
|
|
Homo sapiens |
Hep-G2 Cell |
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; hSIR2, a negative regulator of the p53 protein, showed the opposite effects on the AFP promoter and, like HDAC1, repressed p21 promoter activity. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
ESR1 | up-regulates quantity by expression
transcriptional regulation
|
CDKN1A |
0.491 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-253940 |
|
|
Homo sapiens |
Breast Cancer Cell Line |
pmid |
sentence |
11517191 |
ER beta and ER alpha induced the expression of several endogenous genes such as pS2, TGF alpha, or the cyclin kinase inhibitor p21 but, in contrast to ER alpha, ER beta was unable to regulate c-myc proto-oncogene expression |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MYOD1 | up-regulates
|
CDKN1A |
0.412 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-235831 |
|
|
Mus musculus |
|
pmid |
sentence |
7791789 |
The upregulation of p21 occurred at the levels of mrna and protein, |
|
Publications: |
1 |
Organism: |
Mus Musculus |
Pathways: | Rhabdomyosarcoma |
+ |
RBPJ | up-regulates quantity by expression
transcriptional regulation
|
CDKN1A |
0.313 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-252032 |
|
|
Mus musculus |
|
pmid |
sentence |
15866158 |
Induction of the p21WAF1/Cip1 gene by Notch 1 activation in differentiating keratinocytes is associated with direct targeting of the RBP-J_ protein to the p21 promoter. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
+ |
KLF7 | up-regulates quantity by expression
transcriptional regulation
|
CDKN1A |
0.274 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-224624 |
|
|
Chlorocebus aethiops |
COS Cell |
pmid |
sentence |
14729953 |
KLF7 stimulates p21WAF1/Cip1 transcription |
|
Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
+ |
CDKN1A | down-regulates
binding
|
CDK3 |
0.663 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-29954 |
|
|
Homo sapiens |
|
pmid |
sentence |
7626805 |
P21cip1 is a cyclin-dependent kinase (cdk) inhibitor that is transcriptionally activated by p53 in response to dna damage. We have explored the interaction of p21 with the currently known cdks. p21 effectively inhibits cdk2, cdk3, cdk4, and cdk6 kinases. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
SKP2 | down-regulates
ubiquitination
|
CDKN1A |
0.763 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-138490 |
|
|
Homo sapiens |
|
pmid |
sentence |
15998794 |
Up-regulation of skp2 by notch signaling enhances proteasome-mediated degradation of the ckis, p27 kip1 and p21 cip1, and causes premature entry into s phase. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
SOX9 | up-regulates quantity by expression
transcriptional regulation
|
CDKN1A |
0.383 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255190 |
|
|
Homo sapiens |
Melanoma Cell Line |
pmid |
sentence |
19273910 |
Overexpression of SOX9 in both human and mouse melanoma cell lines induced cell cycle arrest by increasing p21 transcription and restored sensitivity to RA by downregulating expression of PRAME, a melanoma antigen. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
DRAM2 | down-regulates quantity by repression
transcriptional regulation
|
CDKN1A |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-259147 |
|
|
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 |
+ |
MYOD1 | up-regulates quantity by expression
transcriptional regulation
|
CDKN1A |
0.412 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-238529 |
|
|
Mus musculus |
C2C12 Cell |
pmid |
sentence |
10373569 |
Here we report that, at the onset of differentiation, activation by MyoD of the Rb, p21, and cyclin D3 genes occurs in the absence of new protein synthesis and with the requirement of the p300 transcriptional coactivator. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
Pathways: | Rhabdomyosarcoma |
+ |
AR | down-regulates quantity by repression
transcriptional regulation
|
CDKN1A |
0.364 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-253675 |
|
|
Homo sapiens |
LNCaP Cell |
pmid |
sentence |
16281084 |
After AR antagonist flutamide treatment, three hundred and twenty-six genes (3.93%) expressed differentially, 97 down-regulated and 219 up-regulated. Among them, eight up-regulated genes might be cell cycle-related, namely CDC10, NRAS, BTG1, Wee1, CLK3, DKFZP564A122, CDKN1A and BTG2. The CDKN1A and BTG1 gene mRNA expression was confirmed to be higher in the experimental group by RT-PCR, while p53 mRNA expression had no significant changes. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
PBRM1 | up-regulates quantity by expression
transcriptional regulation
|
CDKN1A |
0.266 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-178022 |
|
|
Homo sapiens |
Breast Cancer Cell |
pmid |
sentence |
18339845 |
Endogenous wild-type baf180 bound to the p21 promoter and was required for proper p21 expression and g(1) arrest after transforming growth factor-beta and gamma-radiation treatment. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MDGA2 | up-regulates quantity by expression
transcriptional regulation
|
CDKN1A |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-264242 |
|
|
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 |
+ |
MAGED1 | up-regulates
|
CDKN1A |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-166893 |
|
|
Homo sapiens |
|
pmid |
sentence |
20646279 |
By comparing in vitro differentiation of myoblasts derived from wild-type or maged1 knockout mice, we observed that maged1 deficiency results in reduced levels of p21cip1/waf1, defective cell cycle exit and impaired myotube maturation. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Tissue: |
Myotube |
+ |
TP73 | up-regulates quantity by expression
transcriptional regulation
|
CDKN1A |
0.379 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255468 |
|
|
Homo sapiens |
|
pmid |
sentence |
17700533 |
Dissociation of p73 and HDM2 leads to increased p73 transcriptional activity with upregulation of p73 target genes noxa, puma and p21, as well as enhanced apoptosis. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CDKN1A | up-regulates
|
Cell_cycle_block |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-267286 |
|
|
Homo sapiens |
|
pmid |
sentence |
24470334 |
The cell cycle regulator p21 is induced early in myoblast differentiation and functions to block cell cycle progression |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer |
+ |
CDKN1A | down-regulates
binding
|
CCNB1 |
0.823 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-183498 |
|
|
Homo sapiens |
|
pmid |
sentence |
19158493 |
P21-mediated degradation of cyclin b1 in response to dna damage is necessary for the maintenance of g2 cell cycle arrest. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |