| + |
CHEK2 | up-regulates 
phosphorylation
|
VHL |
0.47 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-177091 |
Ser111 |
GTGRRIHsYRGHLWL |
Homo sapiens |
Kidney Cancer Cell |
| pmid |
sentence |
| 22071692 |
We demonstrated that checkpoint kinase-2 (chk2) binds to the beta-domain of pvhl and phosphorylates ser 111 on dna damage. Notably, this modification enhances pvhl-mediated transactivation of p53 by recruiting p300 and tip60 to the chromatin of p53 target gene |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CHEK2 |
phosphorylation
|
PML |
0.408 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-94872 |
Ser117 |
ESLQRRLsVYRQIVD |
Homo sapiens |
|
| pmid |
sentence |
| 12402044 |
Hcds1/chk2 phosphorylates pml at ser 117 in vitro. hcds1/chk2 phosphorylates pml in vivo. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CHEK2 | down-regulates quantity by destabilization 
phosphorylation
|
CDC25A |
0.838 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-106808 |
Ser124 |
PALKRSHsDSLDHDI |
Homo sapiens |
|
| pmid |
sentence |
| 11298456 |
We show that IR-induced destruction of Cdc25A requires both ATM and the Chk2-mediated phosphorylation of Cdc25A on serine 123. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-99721 |
Ser124 |
PALKRSHsDSLDHDI |
Homo sapiens |
|
| pmid |
sentence |
| 12676583 |
We show that ir-induced destruction of cdc25a requires both atm and the chk2-mediated phosphorylation of cdc25a on serine 123. the basal turnover of cdc25a operating in unperturbed s phase required chk1-dependent phosphorylation of serines 123, 178, 278, and 292. Ir-induced acceleration of cdc25a proteolysis correlated with increased phosphate incorporation into these residues generated by a combined action of chk1 and chk2 kinases. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260778 |
Ser124 |
PALKRSHsDSLDHDI |
Homo sapiens |
|
| pmid |
sentence |
| 11298456 |
We conclude that Chk2-dependent phosphorylation of Cdc25A on Ser 123 represents a critical step in promoting its rapid destruction in response to IR-induced DNA damage. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-99725 |
Ser178 |
LFTQRQNsAPARMLS |
Homo sapiens |
|
| pmid |
sentence |
| 12676583 |
We show that ir-induced destruction of cdc25a requires both atm and the chk2-mediated phosphorylation of cdc25a on serine 123. the basal turnover of cdc25a operating in unperturbed s phase required chk1-dependent phosphorylation of serines 123, 178, 278, and 292. Ir-induced acceleration of cdc25a proteolysis correlated with increased phosphate incorporation into these residues generated by a combined action of chk1 and chk2 kinases. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-118759 |
Ser178 |
LFTQRQNsAPARMLS |
Homo sapiens |
|
| pmid |
sentence |
| 14559997 |
The order and fidelity of cell cycle events in mammals is intimately linked to the integrity of the Chk1 kinase-Cdc25A phosphatase pathway. Chk1 phosphorylation targets Cdc25A for destruction and, as shown here, inhibits interactions between Cdc25A and its mitotic substrate cyclin B1-Cdk1. Phosphorylation of Cdc25A on serine 178 and threonine 507 facilitates 14-3-3 binding, and Chk1 phosphorylates both residues in vitro. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-99729 |
Ser279 |
VLKRPERsQEESPPG |
Homo sapiens |
|
| pmid |
sentence |
| 12676583 |
We show that ir-induced destruction of cdc25a requires both atm and the chk2-mediated phosphorylation of cdc25a on serine 123. the basal turnover of cdc25a operating in unperturbed s phase required chk1-dependent phosphorylation of serines 123, 178, 278, and 292. Ir-induced acceleration of cdc25a proteolysis correlated with increased phosphate incorporation into these residues generated by a combined action of chk1 and chk2 kinases. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-99733 |
Ser293 |
GSTKRRKsMSGASPK |
Homo sapiens |
|
| pmid |
sentence |
| 12676583 |
We show that ir-induced destruction of cdc25a requires both atm and the chk2-mediated phosphorylation of cdc25a on serine 123. the basal turnover of cdc25a operating in unperturbed s phase required chk1-dependent phosphorylation of serines 123, 178, 278, and 292. Ir-induced acceleration of cdc25a proteolysis correlated with increased phosphate incorporation into these residues generated by a combined action of chk1 and chk2 kinases. |
|
| Publications: |
7 |
Organism: |
Homo Sapiens |
| Pathways: | Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition |
| + |
CHEK2 | down-regulates quantity
phosphorylation
|
CDC25A |
0.838 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260835 |
Ser124 |
PALKRSHsDSLDHDI |
Homo sapiens |
|
| pmid |
sentence |
| 12676583 |
Chk2 phosphorylates a subset of the Chk1-targeted sites of Cdc25A | Phosphorylation of serines 123, 178, 278, and 292 regulates both basal and IR-induced accelerated proteolysis of Cdc25A |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260833 |
Ser178 |
LFTQRQNsAPARMLS |
Homo sapiens |
|
| pmid |
sentence |
| 12676583 |
Chk2 phosphorylates a subset of the Chk1-targeted sites of Cdc25A | Phosphorylation of serines 123, 178, 278, and 292 regulates both basal and IR-induced accelerated proteolysis of Cdc25A |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260834 |
Ser279 |
VLKRPERsQEESPPG |
Homo sapiens |
|
| pmid |
sentence |
| 12676583 |
Chk2 phosphorylates a subset of the Chk1-targeted sites of Cdc25A | Phosphorylation of serines 123, 178, 278, and 292 regulates both basal and IR-induced accelerated proteolysis of Cdc25A |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260836 |
Ser293 |
GSTKRRKsMSGASPK |
Homo sapiens |
|
| pmid |
sentence |
| 12676583 |
Chk2 phosphorylates a subset of the Chk1-targeted sites of Cdc25A | Phosphorylation of serines 123, 178, 278, and 292 regulates both basal and IR-induced accelerated proteolysis of Cdc25A |
|
| Publications: |
4 |
Organism: |
Homo Sapiens |
| Pathways: | Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition |
| + |
CHEK2 | up-regulates quantity by stabilization
phosphorylation
|
AATF |
0.366 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264416 |
Ser143 |
SKKSRSHsAKTPGFS |
Homo sapiens |
HCT-116 Cell |
| pmid |
sentence |
| 17157788 |
Three putative Chk2 phosphorylation sites (Stevens et al., 2003) are present in Che-1 at resides Ser141, Ser474, and Ser508. Thus, we performed in vitro Chk2 kinase assays utilizing the GST-Che-1 fusion peptides spanning these residues as substrates.| Taken together, these results indicate that Chk2 phosphorylates Che-1 and this phosphorylation contributes to increase Che-1 stability. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264417 |
Ser477 |
ELIERKTsSLDPNDQ |
Homo sapiens |
HCT-116 Cell |
| pmid |
sentence |
| 17157788 |
Three putative Chk2 phosphorylation sites (Stevens et al., 2003) are present in Che-1 at resides Ser141, Ser474, and Ser508. Thus, we performed in vitro Chk2 kinase assays utilizing the GST-Che-1 fusion peptides spanning these residues as substrates.| Taken together, these results indicate that Chk2 phosphorylates Che-1 and this phosphorylation contributes to increase Che-1 stability. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264418 |
Ser510 |
KKVDRKAsKGRKLRF |
Homo sapiens |
HCT-116 Cell |
| pmid |
sentence |
| 17157788 |
Three putative Chk2 phosphorylation sites (Stevens et al., 2003) are present in Che-1 at resides Ser141, Ser474, and Ser508. Thus, we performed in vitro Chk2 kinase assays utilizing the GST-Che-1 fusion peptides spanning these residues as substrates.| Taken together, these results indicate that Chk2 phosphorylates Che-1 and this phosphorylation contributes to increase Che-1 stability. |
|
| Publications: |
3 |
Organism: |
Homo Sapiens |
| + |
CHEK2 | up-regulates quantity by stabilization
phosphorylation
|
TP53 |
0.785 |
| 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-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-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-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-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-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-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-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-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-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. |
|
| 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. |
|
| Publications: |
18 |
Organism: |
Homo Sapiens |
| Pathways: | FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer |
| + |
ATM | up-regulates activity
phosphorylation
|
CHEK2 |
0.831 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-81391 |
Ser19 |
SHGSSACsQPHGSVT |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 10973490 |
Phosphorylation and activation of chk2 are ataxia telangiectasia-mutated (atm) dependent in response to ir |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-81395 |
Ser28 |
PHGSVTQsQGSSSQS |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 10973490 |
Phosphorylation and activation of chk2 are ataxia telangiectasia-mutated (atm) dependent in response to irser28 was also found to be phosphorylated in an atm-dependent manner |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-81399 |
Ser33 |
TQSQGSSsQSQGISS |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 10973490 |
Phosphorylation and activation of chk2 are ataxia telangiectasia-mutated (atm) dependent in response to ir |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-81403 |
Ser35 |
SQGSSSQsQGISSSS |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 10973490 |
Phosphorylation and activation of chk2 are ataxia telangiectasia-mutated (atm) dependent in response to ir |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-81407 |
Ser50 |
TSTMPNSsQSSHSSS |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 10973490 |
Phosphorylation and activation of chk2 are ataxia telangiectasia-mutated (atm) dependent in response to iratm- and rad3-related also phosphorylates thr68 in addition to thr26 and ser50, which are not phosphorylated to a significant extent by atm in vitro. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-87850 |
Thr26 |
SQPHGSVtQSQGSSS |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 12024051 |
We show here that autophosphorylation of chk2 produced in a cell-free system requires trans phosphorylation by a wortmannin-sensitive kinase, probably atm or atr |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-81438 |
Thr68 |
SSLETVStQELYSIP |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 10973490 |
Here we show that in vitro, atm phosphorylates the ser-gln/thr-gln (sq/tq) cluster domain (scd) on chk2, which contains seven sq/tq motifs, and thr68 is the major in vitro phosphorylation site by atm. Atm predominantly phosphorylates chk2 at thr68, promoting homodimerization and activation via intramolecular trans-autophosphorylation at thr383/387. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-276053 |
Thr68 |
SSLETVStQELYSIP |
in vitro |
|
| pmid |
sentence |
| 16481012 |
Plk3 phosphorylates Chk2 at two residues, serine 62 (S62) and serine 73 (S73) in vitro, and this phosphorylation facilitates subsequent phosphorylation of Chk2 on T68 by ATM in response to DNA damage. When the Chk2 mutant construct GFP-Chk2 S73A (serine 73 mutated to alanine) is transfected into cells, it no longer associates with a large complex in vivo, and manifests a significant reduction in kinase activity. |
|
| Publications: |
8 |
Organism: |
Homo Sapiens, In Vitro |
| Pathways: | DNA repair in cancer, FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer |
| + |
CHEK2 | up-regulates activity
phosphorylation
|
TP53 |
0.785 |
| 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 |
| + |
CHEK2 | down-regulates activity
phosphorylation
|
CDC25C |
0.852 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-102779 |
Ser216 |
SGLYRSPsMPENLNR |
Homo sapiens |
|
| pmid |
sentence |
| 12835754 |
Activated chk2 in turn phosphorylates cdc25c at serine-216 contributing to the g2/m checkpoints. Cds1 phosphorylates and inactivates cdc25 in vitro|CDC25C is phosphorylated on Ser 216 throughout interphase, but not in mitosis. This creates a binding site for 14‐3‐3 proteins | It has been suggested that 14‐3‐3 protein binding is responsible for retaining Cdc25C in the cytoplasm during interphase, thereby contributing to the prevention of premature initiation of mitotic events |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CHEK2 | up-regulates activity
phosphorylation
|
PSME3 |
0.355 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273611 |
Ser247 |
EKIKRPRsSNAETLY |
Homo sapiens |
U2-OS Cell |
| pmid |
sentence |
| 25361978 |
REGγ interacts with DBC1 and is phosphorylated by Chk2. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CHEK2 | down-regulates
phosphorylation
|
RASGRF1 |
0.373 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-150843 |
Ser287 |
PITHDDVsSIFLNSE |
Homo sapiens |
|
| pmid |
sentence |
| 17110335 |
During interphase, cdc25 is inhibited by ser287 phosphorylation (xenopus cdc25;ser 216 in human cdc25c) and this inhibitory phosphorylation is maintained by dna-responsive checkpoints / s287 is targeted by many kinases, including chk1, chk2, ctak-1, pka, p38 and mapkap kinase-2 suggesting that phosphorylation of this site may integrate multiple signaling inputs. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CHEK2 | down-regulates
phosphorylation
|
MDM4 |
0.712 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-140417 |
Ser342 |
SKLTHSLsTSDITAI |
Homo sapiens |
|
| pmid |
sentence |
| 16163388 |
Phosphorylation of s342 and s367 in vivo require the chk2 kinase. Chk2 also stimulates mdmx ubiquitination and degradation by mdm2 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CHEK2 | up-regulates quantity by stabilization
phosphorylation
|
E2F1 |
0.504 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-197278 |
Ser364 |
PLLSRMGsLRAPVDE |
Homo sapiens |
|
| pmid |
sentence |
| 22558186 |
Among these effector proteins, chk1 phosphorylates tlk12 and rad51, while brca, pik3, pml and e2f1 are chk2 substrates. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-100898 |
Ser364 |
PLLSRMGsLRAPVDE |
Homo sapiens |
|
| pmid |
sentence |
| 12717439 |
We report that checkpoint kinase 2 (chk2) regulates e2f-1 activity in response to the dna-damaging agent etoposide. A chk2 consensus phosphorylation site in e2f-1 is phosphorylated in response to dna damage |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition |
| + |
CHEK2 | up-regulates activity
phosphorylation
|
E2F1 |
0.504 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260822 |
Ser364 |
PLLSRMGsLRAPVDE |
Homo sapiens |
|
| pmid |
sentence |
| 12717439 |
Therefore, Chk2 phosphorylates and activates E2F-1 in response to DNA damage, resulting in apoptosis. | These results suggest that the Ser 364 site is phosphorylated by Chk2 and that anti-P-Ser 364 recognises the phosphorylated site in E2F-1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition |
| + |
CHEK2 | down-regulates quantity by destabilization
phosphorylation
|
MDM4 |
0.712 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-178071 |
Ser367 |
PDCRRTIsAPVVRPK |
Homo sapiens |
|
| pmid |
sentence |
| 18356162 |
The chk1 and chk2 kinases have also been shown to phosphorylate ser367, leading to 14-3-3 binding (34_36, 38, 44). In both cases, the outcome differed: in chk1-mediated phosphorylation, mdmx was translocated to the cytoplasm;in chk2-mediated phosphorylation, mdmx was degraded (34_36, 38, 44). It is possible that the damage response is mediated through additional phosphorylation sites other than ser367 and that, depending on the type of damage, certain sites will be modified, leading to different outcomes. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CHEK2 | up-regulates
phosphorylation
|
FOXM1 |
0.709 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-150746 |
Ser376 |
PLLPRVSsYLVPIQF |
Homo sapiens |
U2-OS Cell |
| pmid |
sentence |
| 17101782 |
Chk2 mediates stabilization of the foxm1 transcription factor to stimulate expression of dna repair genesthis phosphorylation of foxm1 on serine residue 361 caused increased stability of the foxm1 protein |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CHEK2 | up-regulates activity
phosphorylation
|
CHEK2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-179537 |
Ser379 |
SKILGETsLMRTLCG |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 18644861 |
Regulation of chk2 ubiquitination and signaling through autophosphorylation of serine 379.Thus, auto-/transphosphorylation of s379 is required for chk2 ubiquitination and effector function |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-103544 |
Ser516 |
PQVLAQPsTSRKRPR |
Homo sapiens |
HCT-15 Cell |
| pmid |
sentence |
| 12855706 |
Chk2 is also autophosphorylated following dna damage. It is proposed that autophosphorylation of chk2 may contribute to chk2 activation. To fully understand the regulation of chk2, we mapped an in vitro chk2 autophosphorylation site at c-terminal serine 516 site (ser-516). Ser-516 of chk2 is phosphorylated following radiation in vivo, and this phosphorylation depends on the kinase activity of chk2. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-116127 |
Thr383 |
GETSLMRtLCGTPTY |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 11901158 |
Phosphorylation of thr-68 by the ataxia telangiectasia-mutated is necessary for efficient activation of chk2 when cells are exposed to ionizing radiation. By an unknown mechanism, this initial event promotes additional autophosphorylation events including modifications of thr-383 and thr-387 |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-116131 |
Thr387 |
LMRTLCGtPTYLAPE |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 11901158 |
Phosphorylation of thr-68 by the ataxia telangiectasia-mutated is necessary for efficient activation of chk2 when cells are exposed to ionizing radiation. By an unknown mechanism, this initial event promotes additional autophosphorylation events including modifications of thr-383 and thr-387 |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-116135 |
Thr68 |
SSLETVStQELYSIP |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 11901158 |
Thus, activation of chk2 in irradiated cells may occur through oligomerization of chk2 via binding of the thr-68-phosphorylated region of one chk2 to the fha domain of another. Oligomerization of chk2 may therefore increase the efficiency of trans-autophosphorylation resulting in the release of active chk2 monomers that proceed to enforce checkpoint control in irradiated cells. |
|
| Publications: |
5 |
Organism: |
Homo Sapiens |
| Pathways: | DNA repair in cancer, FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer |
| + |
CHEK2 | down-regulates
phosphorylation
|
MAPT |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-171026 |
Ser579 |
NVKSKIGsTENLKHQ |
Homo sapiens |
|
| pmid |
sentence |
| 21215781 |
Tau pseudophosphorylation at specific sites such as s262, s293, s324 and s356 was reported to induce tau conformational change and attenuate tau binding to microtubules (fischer et al., 2009). Then, newly soluble tau proteins are targeted by post-translational modifications that directly or indirectly alter tau conformation, promoting tau dimerization in an anti-parallel manner. Stable tau dimers form tau oligomers, which continue in the aggregation process |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CHEK2 | up-regulates activity
phosphorylation
|
SOD1 |
0.387 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262794 |
Ser60 |
DNTAGCTsAGPHFNP |
Saccharomyces cerevisiae |
|
| pmid |
sentence |
| 24647101 |
ROS signaling is mediated by Mec1/ATM and its effector Dun1/Cds1 kinase, through Dun1 interaction with Sod1 and regulation of Sod1 by phosphorylation at S60, 99. In the nucleus, Sod1 binds to the promoters and regulates the expression of oxidative resistance and repair genes. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262795 |
Ser99 |
KDGVADVsIEDSVIS |
Saccharomyces cerevisiae |
|
| pmid |
sentence |
| 24647101 |
ROS signaling is mediated by Mec1/ATM and its effector Dun1/Cds1 kinase, through Dun1 interaction with Sod1 and regulation of Sod1 by phosphorylation at S60, 99. In the nucleus, Sod1 binds to the promoters and regulates the expression of oxidative resistance and repair genes. |
|
| Publications: |
2 |
Organism: |
Saccharomyces Cerevisiae |
| + |
CHEK2 | up-regulates activity
phosphorylation
|
RB1 |
0.435 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-153908 |
Ser612 |
MYLSPVRsPKKKGST |
Homo sapiens |
MCF-7 Cell |
| pmid |
sentence |
| 17380128 |
Phosphorylation of prb at ser612 by chk1/2 leads to a complex between prb and e2f-1 after dna damageprb inhibits cell cycle progression through interactions with the e2f family of transcription factors. Here, we report that dna damage induced not only the dephosphorylation of prb at cdk phosphorylation sites and the binding of prb to e2f-1, but also the phosphorylation of prb at ser612. Phosphorylation of prb at ser612 enhanced the formation of a complex between prb and e2f-1 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer |
| + |
PLK3 | up-regulates activity
phosphorylation
|
CHEK2 |
0.64 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-276052 |
Ser62 |
SSSGTLSsLETVSTQ |
in vitro |
|
| pmid |
sentence |
| 16481012 |
Plk3 phosphorylates Chk2 at two residues, serine 62 (S62) and serine 73 (S73) in vitro, and this phosphorylation facilitates subsequent phosphorylation of Chk2 on T68 by ATM in response to DNA damage. When the Chk2 mutant construct GFP-Chk2 S73A (serine 73 mutated to alanine) is transfected into cells, it no longer associates with a large complex in vivo, and manifests a significant reduction in kinase activity. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-276051 |
Ser73 |
VSTQELYsIPEDQEP |
in vitro |
|
| pmid |
sentence |
| 16481012 |
Plk3 phosphorylates Chk2 at two residues, serine 62 (S62) and serine 73 (S73) in vitro, and this phosphorylation facilitates subsequent phosphorylation of Chk2 on T68 by ATM in response to DNA damage. When the Chk2 mutant construct GFP-Chk2 S73A (serine 73 mutated to alanine) is transfected into cells, it no longer associates with a large complex in vivo, and manifests a significant reduction in kinase activity. |
|
| Publications: |
2 |
Organism: |
In Vitro |
| + |
CHEK2 | up-regulates activity
phosphorylation
|
BECN1 |
0.305 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264557 |
Ser90 |
IPPARMMsTESANSF |
Homo sapiens |
NCI-H1299 Cell |
| pmid |
sentence |
| 32187724 |
We report that CHK2 binds to and phosphorylates Beclin 1 at Ser90/Ser93, thereby impairing Beclin 1-Bcl-2 autophagy-regulatory complex formation in a ROS-dependent fashion.|CHK2 binds to and phosphorylates Beclin 1 at Ser90/Ser93, promoting autophagy via Beclin 1 release from Bcl‐2 sequestration |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264556 |
Ser93 |
ARMMSTEsANSFTLI |
Homo sapiens |
NCI-H1299 Cell |
| pmid |
sentence |
| 32187724 |
We report that CHK2 binds to and phosphorylates Beclin 1 at Ser90/Ser93, thereby impairing Beclin 1-Bcl-2 autophagy-regulatory complex formation in a ROS-dependent fashion.|CHK2 binds to and phosphorylates Beclin 1 at Ser90/Ser93, promoting autophagy via Beclin 1 release from Bcl‐2 sequestration |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
CHEK2 | up-regulates
phosphorylation
|
BRCA1 |
0.78 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-120575 |
Ser988 |
PPLFPIKsFVKTKCK |
Homo sapiens |
Breast Cancer Cell |
| pmid |
sentence |
| 14701743 |
In this study, we tested the hypothesis that the brca1-mediated regulation of recombination requires the chk2- and atm-dependent phosphorylation sites. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | DNA repair in cancer, Cell cycle: G2/M phase transition |
| + |
PLK1 |
phosphorylation
|
CHEK2 |
0.506 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249180 |
Thr26 |
SQPHGSVtQSQGSSS |
in vitro |
|
| pmid |
sentence |
| 12493754 |
Plk1 overexpression enhances phosphorylation of Chk2 at Thr-68. Plk1 phosphorylates recombinant Chk2 in vitro. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
CHEK2 | up-regulates
phosphorylation
|
XRCC1 |
0.536 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-181816 |
Thr284 |
APTRTPAtAPVPARA |
Homo sapiens |
|
| pmid |
sentence |
| 18971944 |
Chk2 formed a complex with xrcc1, the ber scaffold protein, and phosphorylated xrcc1 in vivo and in vitro at thr(284). our results are consistent with the phosphorylation of xrcc1 by atm-chk2 facilitating recruitment of downstream ber proteins to the initial damage recognition/excision step to promote ber. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CHEK2 |
phosphorylation
|
TTK |
0.298 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-183470 |
Thr288 |
SPDCDVKtDDSVVPC |
Homo sapiens |
|
| pmid |
sentence |
| 19151762 |
Phosphorylation at ttk/hmps1 thr288 is enhanced by chk2 in vitro and in vivo after ir |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CHEK2 | up-regulates
phosphorylation
|
TTK |
0.298 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-242665 |
Thr288 |
SPDCDVKtDDSVVPC |
Homo sapiens |
|
| pmid |
sentence |
| 19151762 |
Phosphorylation at ttk/hmps1 thr288 is enhanced by chk2 in vitro and in vivo after ir |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TTK | up-regulates
phosphorylation
|
CHEK2 |
0.298 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-132665 |
Thr68 |
SSLETVStQELYSIP |
Homo sapiens |
|
| pmid |
sentence |
| 15618221 |
Ttk/hmps1 directly phosphorylates chk2 on thr-68 in vitro.ablation of ttk expression using small interfering rna results not only in reduced chk2 thr-68 phosphorylation, but also in impaired growth arrest. Our results are consistent with a model in which ttk functions upstream from chk2 in response to dna damage |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PRKDC | up-regulates
phosphorylation
|
CHEK2 |
0.615 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-133384 |
Thr68 |
SSLETVStQELYSIP |
Homo sapiens |
|
| pmid |
sentence |
| 15668230 |
We have found that dna-pk is the major constituent of an activity present in extracts of mammalian cells that phosphorylates chk2. Our results suggest that hypophosphorylated chk2 can be phosphorylated at thr68 by dna-pk in vitro. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Cell cycle: G2/M phase transition |
| + |
PPP2CB | up-regulates activity
dephosphorylation
|
CHEK2 |
0.314 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-248582 |
Thr68 |
SSLETVStQELYSIP |
Homo sapiens |
|
| pmid |
sentence |
| 16596250 |
Protein phosphatase 2A interacts with Chk2 and regulates phosphorylation at Thr-68 after cisplatin treatment of human ovarian cancer cells|In response to DNA damage, Chk2 is initially phosphorylated at Thr-68, which leads to its full activation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATR | up-regulates activity
phosphorylation
|
CHEK2 |
0.856 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-81442 |
Thr68 |
SSLETVStQELYSIP |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 10973490 |
Atm- and rad3-related also phosphorylates thr68 in addition to thr26 and ser50, which are not phosphorylated to a significant extent by atm in vitro.Substitution of thr68 with ala reduced the extent of phosphorylation and activation of chk2 in response to ir |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | DNA repair in cancer, FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer |
| + |
PPP2CA | up-regulates activity
dephosphorylation
|
CHEK2 |
0.443 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-248617 |
Thr68 |
SSLETVStQELYSIP |
Homo sapiens |
Ovary Cancer Cell |
| pmid |
sentence |
| 16596250 |
Protein phosphatase 2A interacts with Chk2 and regulates phosphorylation at Thr-68 after cisplatin treatment of human ovarian cancer cells|In response to DNA damage, Chk2 is initially phosphorylated at Thr-68, which leads to its full activation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PLK1 | up-regulates
phosphorylation
|
CHEK2 |
0.506 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-96637 |
Thr68 |
SSLETVStQELYSIP |
Homo sapiens |
|
| pmid |
sentence |
| 12493754 |
Plk1 overexpression enhances phosphorylation of chk2 at thr-68. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PPM1D | up-regulates activity
dephosphorylation
|
CHEK2 |
0.596 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-248318 |
Thr68 |
SSLETVStQELYSIP |
in vitro |
|
| pmid |
sentence |
| 16311512 |
an in vitro phosphatase assay revealed that Wip1 (WT), but not Wip1 (D314A), dephosphorylates Thr68 on phosphorylated Chk2 in vitro, resulting in the inhibition of Chk2 kinase activity toward glutathione S-transferase-Cdc25C. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
CHEK2 | up-regulates
phosphorylation
|
PPP2R5C |
0.326 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-129255 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 15380617 |
Found that chk2 associated with the b' regulatory subunit of protein phosphatase pp2a. In vitro kinase assays showed that b'gamma3 was a potent chk2 substrate. This phosphorylation increased the catalytic phosphatase activity of pp2a. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
3-(carbamoylamino)-5-(3-fluorophenyl)-N-[(3S)-3-piperidinyl]-2-thiophenecarboxamide | down-regulates
chemical inhibition
|
CHEK2 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-190206 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-163119 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20068082 |
Azd7762 is equally potent against chk2 in vitro. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
NatA | down-regulates activity
acetylation
|
CHEK2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267228 |
|
|
Homo sapiens |
HCT-116 Cell |
| pmid |
sentence |
| 21351257 |
The human protein N(α)-terminal acetyltransferase A complex (hNatA), composed of the catalytic hNaa10p (hArd1) and auxiliary hNaa15p (hNat1/NATH/Tubedown) subunits, was reported to be important for cell survival and growth of various types of cancer. lack of acetylation by hNatA activated H2A.X and Chk2 in both HCT116 cell lines independent of TP53 status (Fig. 6). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
XRCC3 | up-regulates activity 
|
CHEK2 |
0.533 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263261 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 23438602 |
Interestingly, as with ATM (40, 41), XRCC3-deficient cells exhibited RDS and impaired CHK2 activation|Notably, early activation of CHK2 in S/G2 phase was downstream of XRCC3 recruitment as well as its phosphorylation at the sites of DSBs. NBS1 also has been shown to be involved in the early activation of CHK2 in response to IR (42). It is likely that NBS1-dependent CHK2 phosphorylation is mediated through XRCC3 activation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
6-bromo-3-(1-methyl-4-pyrazolyl)-5-(3-piperidinyl)-7-pyrazolo[1,5-a]pyrimidinamine | down-regulates
chemical inhibition
|
CHEK2 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-206841 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
D1-D2-G-X3 complex | up-regulates activity
|
CHEK2 |
0.494 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263262 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 23438602 |
Interestingly, as with ATM (40, 41), XRCC3-deficient cells exhibited RDS and impaired CHK2 activation|Notably, early activation of CHK2 in S/G2 phase was downstream of XRCC3 recruitment as well as its phosphorylation at the sites of DSBs. NBS1 also has been shown to be involved in the early activation of CHK2 in response to IR (42). It is likely that NBS1-dependent CHK2 phosphorylation is mediated through XRCC3 activation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SCHEMBL14517914 | down-regulates
chemical inhibition
|
CHEK2 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-163234 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20068082 |
Xl844 (exelixis) a potent atp-competitive inhibitor of chk1 (ki, 2.2nm) and chk2 (ki, 0.07nm). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
DNA_damage | up-regulates activity
|
CHEK2 |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-242605 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19151762 |
Cell cycle progression is monitored constantly to ensure faithful passage of genetic codes and genome stability. We have demonstrated previously that, upon DNA damage, TTK/hMps1 activates the checkpoint kinase CHK2 by phosphorylating CHK2 at Thr68 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | DNA repair in cancer, FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer |
| + |
CHEK2 | up-regulates
phosphorylation
|
KIT |
0.293 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-197281 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22558186 |
In this report, we characterize the binding of sh2(chk) to specific phosphotyrosine sites on the c-kit protein sequence. the sh2(chk) binding to the two sites is direct and not through phosphorylated intermediates such as fyn or shc. this indicates that chk binds to the same site on c-kit to which fyn binds, possibly bringing the two into proximity on associated c-kit subunits and leading to the down-regulation of fyn by chk. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
3.0
CHEK2
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