+ |
CHEK1 | down-regulates activity
phosphorylation
|
E2F6 |
0.557 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-266370 |
Ser12 |
RPARKLPsLLLDPTE |
in vitro |
|
pmid |
sentence |
23954429 |
the checkpoint kinase Chk1 phosphorylates E2F6 leading to its dissociation from promoters. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-266371 |
Ser52 |
EDNVQYVsMRKALKV |
in vitro |
|
pmid |
sentence |
23954429 |
the checkpoint kinase Chk1 phosphorylates E2F6 leading to its dissociation from promoters. |
|
Publications: |
2 |
Organism: |
In Vitro |
+ |
CHEK1 | up-regulates
phosphorylation
|
E2F3 |
0.335 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-161758 |
Ser124 |
PALGRGGsGGGGGPP |
Homo sapiens |
|
pmid |
sentence |
19917728 |
These results suggest that e2f3a is directly phosphorylated by chk kinases and that the phosphorylation of serine 124 is required for the posttranslational induction of e2f3a protein by chemotherapy. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CHEK1 | down-regulates
phosphorylation
|
CDC25A |
0.852 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-163134 |
Ser124 |
PALKRSHsDSLDHDI |
Homo sapiens |
|
pmid |
sentence |
20068082 |
The signal for ubiquitination after uv and ir exposure is created by phosphorylation of cdc25a mediated by chk1 and chk2, respectively. Chk1 is a major kinase phosphorylating cdc25a (ser76/124) and cdc25c (ser216). |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-163138 |
Ser178 |
LFTQRQNsAPARMLS |
Homo sapiens |
|
pmid |
sentence |
20068082 |
The signal for ubiquitination after uv and ir exposure is created by phosphorylation of cdc25a mediated by chk1 and chk2, respectively. Chk1 is a major kinase phosphorylating cdc25a (ser76/124) and cdc25c (ser216). regulation;btrc(induces);14-3-3 beta(induces);apoptosis, altered;14-3-3 beta(induces);ccna1(disrupts);cdk2(disrupts);cdk1(disrupts);ccnb1(disrupts); |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-163142 |
Ser279 |
VLKRPERsQEESPPG |
Homo sapiens |
|
pmid |
sentence |
20068082 |
The signal for ubiquitination after uv and ir exposure is created by phosphorylation of cdc25a mediated by chk1 and chk2, respectively. Chk1 is a major kinase phosphorylating cdc25a (ser76/124) and cdc25c (ser216). regulation;btrc(induces);14-3-3 beta(induces);apoptosis, altered;14-3-3 beta(induces);ccna1(disrupts);cdk2(disrupts);cdk1(disrupts);ccnb1(disrupts); |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-163146 |
Ser293 |
GSTKRRKsMSGASPK |
Homo sapiens |
|
pmid |
sentence |
20068082 |
The signal for ubiquitination after uv and ir exposure is created by phosphorylation of cdc25a mediated by chk1 and chk2, respectively. Chk1 is a major kinase phosphorylating cdc25a (ser76/124) and cdc25c (ser216). |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-163150 |
Ser76 |
SNLQRMGsSESTDSG |
Homo sapiens |
|
pmid |
sentence |
20068082 |
The signal for ubiquitination after uv and ir exposure is created by phosphorylation of cdc25a mediated by chk1 and chk2, respectively. Chk1 is a major kinase phosphorylating cdc25a (ser76/124) and cdc25c (ser216). regulation;btrc(induces);14-3-3 beta(induces);apoptosis, altered;14-3-3 beta(induces);ccna1(disrupts);cdk2(disrupts);cdk1(disrupts);ccnb1(disrupts); |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-163154 |
Thr507 |
KFRTKSRtWAGEKSK |
Homo sapiens |
|
pmid |
sentence |
20068082 |
The signal for ubiquitination after uv and ir exposure is created by phosphorylation of cdc25a mediated by chk1 and chk2, respectively. Chk1 is a major kinase phosphorylating cdc25a (ser76/124) and cdc25c (ser216). regulation;btrc(induces);14-3-3 beta(induces);apoptosis, altered;14-3-3 beta(induces);ccna1(disrupts);cdk2(disrupts);cdk1(disrupts);ccnb1(disrupts); |
|
Publications: |
6 |
Organism: |
Homo Sapiens |
Pathways: | Cell cycle: G2/M phase transition |
+ |
CHEK1 | up-regulates activity
phosphorylation
|
TP53 |
0.772 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-217791 |
Ser15 |
PSVEPPLsQETFSDL |
Homo sapiens |
LNCaP Cell |
pmid |
sentence |
15659650 |
CHK1 and CHK2 phosphorylate the p53 N terminus at Ser15, Thr18, Ser20, and Ser37 |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-217795 |
Ser20 |
PLSQETFsDLWKLLP |
Homo sapiens |
LNCaP Cell |
pmid |
sentence |
15659650 |
CHK1 and CHK2 phosphorylate the p53 N terminus at Ser15, Thr18, Ser20, and Ser37 |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-217853 |
Ser366 |
PGGSRAHsSHLKSKK |
Homo sapiens |
LNCaP Cell |
pmid |
sentence |
15659650 |
Phosphorylation by chk1 of at least three of these sites, Ser366, Ser378, and Thr387, was induced by DNA damage. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-217799 |
Ser37 |
NVLSPLPsQAMDDLM |
Homo sapiens |
LNCaP Cell |
pmid |
sentence |
15659650 |
CHK1 and CHK2 phosphorylate the p53 N terminus at Ser15, Thr18, Ser20, and Ser37 |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-217857 |
Ser378 |
SKKGQSTsRHKKLMF |
Homo sapiens |
|
pmid |
sentence |
15659650 |
Phosphorylation by chk1 of at least three of these sites, Ser366, Ser378, and Thr387, was induced by DNA damage. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-217803 |
Thr18 |
EPPLSQEtFSDLWKL |
Homo sapiens |
|
pmid |
sentence |
15659650 |
CHK1 and CHK2 phosphorylate the p53 N terminus at Ser15, Thr18, Ser20, and Ser37 |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-217861 |
Thr387 |
HKKLMFKtEGPDSD |
Homo sapiens |
LNCaP Cell |
pmid |
sentence |
15659650 |
Phosphorylation by chk1 of at least three of these sites, Ser366, Ser378, and Thr387, was induced by DNA damage. |
|
Publications: |
7 |
Organism: |
Homo Sapiens |
Pathways: | FLT3-ITD signaling, Cell cycle: G2/M phase transition |
+ |
CHEK1 | up-regulates activity
phosphorylation
|
ASF1A |
0.424 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-277620 |
Ser166 |
KLEDAESsNPNLQSL |
Homo sapiens |
HEK-293T Cell |
pmid |
sentence |
33503415 |
Chk1 activated by ataxia telangiectasia mutated (ATM) kinase on DNA breaks in G1 promotes NHEJ through direct phosphorylation of ASF1A at Ser-166. ASF1A phosphorylated at Ser-166 interacts with the repair protein MDC1 and thus enhances MDC1's interaction with ATM and the stable localization of ATM at DNA breaks. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CHEK1 |
phosphorylation
|
RASSF1 |
0.36 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-203144 |
Ser188 |
PSSKKPPsLQDARRG |
Homo sapiens |
|
pmid |
sentence |
24197116 |
This study reveals that chk1-mediated phosphorylation of rassf1a, at serine 184, plays an important role in cell-cycle regulation |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CHEK1 | down-regulates quantity by destabilization
phosphorylation
|
CDC25C |
0.845 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-163158 |
Ser216 |
SGLYRSPsMPENLNR |
Homo sapiens |
|
pmid |
sentence |
20068082 |
The signal for ubiquitination after uv and ir exposure is created by phosphorylation of cdc25a mediated by chk1 and chk2, respectively. Chk1 is a major kinase phosphorylating cdc25a (ser76/124) and cdc25c (ser216). |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CHEK1 | down-regulates activity
phosphorylation
|
CDC25B |
0.781 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-149898 |
Ser230 |
AFAQRPSsAPDLMCL |
Homo sapiens |
|
pmid |
sentence |
17003105 |
Here, we show that cdc25b is phosphorylated by chk1 in vitro on multiple residues, including s230 and s563.We show that the s230-phosphorylated form of cdc25b is located at the centrosome from early s phase until mitosis. Furthermore, mutation of s230 to alanine increases the mitotic-inducing activity of cdc25b |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CHEK1 | down-regulates activity
phosphorylation
|
ERRFI1 |
0.331 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-276411 |
Ser251 |
RRLRRSHsGPAGSFN |
in vitro |
|
pmid |
sentence |
22505024 |
Our results suggest that Chk1 phosphorylates Mig-6 on Ser 251, resulting in the inhibition of Mig-6, and that Chk1 acts as a positive regulator of EGF signalling. This is a novel function of Chk1. |
|
Publications: |
1 |
Organism: |
In Vitro |
+ |
CHEK1 | up-regulates
phosphorylation
|
NEK11 |
0.267 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-187863 |
Ser273 |
SMLNKNPsLRPSAIE |
Homo sapiens |
|
pmid |
sentence |
19734889 |
We demonstrate that chk1 (checkpoint kinase 1) directly activates nek11 by phosphorylating it on ser 273 |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
AKT1 | down-regulates
phosphorylation
|
CHEK1 |
0.441 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-124365 |
Ser280 |
AKRPRVTsGGVSESP |
Homo sapiens |
|
pmid |
sentence |
15107605 |
The chk1 protein phosphorylated by pkb on serine 280 does not enter into protein complexes after replication arrest. Moreover, chk1 phosphorylated by pkb fails to undergo activating phosphorylation on serine 345 by atm/atr. Phosphorylation by atm/atr and association with other checkpoint proteins are essential steps in activation of chk1. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | FLT3-ITD signaling |
+ |
AKT | down-regulates
phosphorylation
|
CHEK1 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-244206 |
Ser280 |
AKRPRVTsGGVSESP |
Homo sapiens |
|
pmid |
sentence |
15107605 |
The chk1 protein phosphorylated by pkb on serine 280 does not enter into protein complexes after replication arrest. Moreover, chk1 phosphorylated by pkb fails to undergo activating phosphorylation on serine 345 by atm/atr. Phosphorylation by atm/atr and association with other checkpoint proteins are essential steps in activation of chk1. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | FLT3-ITD signaling, Cell cycle: G2/M phase transition |
+ |
CDK1 | up-regulates
phosphorylation
|
CHEK1 |
0.419 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-175071 |
Ser286 |
TSGGVSEsPSGFSKH |
Homo sapiens |
|
pmid |
sentence |
21765472 |
Chk1 itself is also subject to cdk-mediated phosphorylation at serines 286 and 301 (s286 and 301). We show that chk1 s301 phosphorylation increases as cells progress through s and g2 and that both cdk1 and cdk2 are likely to contribute to this modification in vivo. We also find that substitution of s286 and s301 with non-phosphorylatable alanine residues strongly attenuates dna damage-induced chk1 activation and g2 checkpoint proficiency |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-175075 |
Ser301 |
IQSNLDFsPVNSASS |
Homo sapiens |
|
pmid |
sentence |
21765472 |
Chk1 itself is also subject to cdk-mediated phosphorylation at serines 286 and 301 (s286 and 301). We show that chk1 s301 phosphorylation increases as cells progress through s and g2 and that both cdk1 and cdk2 are likely to contribute to this modification in vivo. We also find that substitution of s286 and s301 with non-phosphorylatable alanine residues strongly attenuates dna damage-induced chk1 activation and g2 checkpoint proficiency |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
CDK2 | up-regulates
phosphorylation
|
CHEK1 |
0.535 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-175079 |
Ser286 |
TSGGVSEsPSGFSKH |
Homo sapiens |
|
pmid |
sentence |
21765472 |
Chk1 itself is also subject to cdk-mediated phosphorylation at serines 286 and 301 (s286 and 301). We show that chk1 s301 phosphorylation increases as cells progress through s and g2 and that both cdk1 and cdk2 are likely to contribute to this modification in vivo. We also find that substitution of s286 and s301 with non-phosphorylatable alanine residues strongly attenuates dna damage-induced chk1 activation and g2 checkpoint proficiency |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-175083 |
Ser301 |
IQSNLDFsPVNSASS |
Homo sapiens |
|
pmid |
sentence |
21765472 |
Chk1 itself is also subject to cdk-mediated phosphorylation at serines 286 and 301 (s286 and 301). We show that chk1 s301 phosphorylation increases as cells progress through s and g2 and that both cdk1 and cdk2 are likely to contribute to this modification in vivo. We also find that substitution of s286 and s301 with non-phosphorylatable alanine residues strongly attenuates dna damage-induced chk1 activation and g2 checkpoint proficiency |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
CHEK1 | down-regulates
phosphorylation
|
SYK |
0.316 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-197528 |
Ser295 |
GIISRIKsYSFPKPG |
Homo sapiens |
|
pmid |
sentence |
22585575 |
We found that chk1 phosphorylated the tumor suppressor spleen tyrosine kinase (l) (syk[l]) and identified the phosphorylation site at ser295. Furthermore, chk1 phosphorylation of syk(l) promoted its subsequent proteasomal degradation. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CHEK1 | up-regulates activity
phosphorylation
|
CHEK1 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-219240 |
Ser296 |
GFSKHIQsNLDFSPV |
Xenopus laevis |
|
pmid |
sentence |
15707391 |
This suggests that Ser296 is probably one of the sites autophosphorylated when Chk1 is fully activated [21], despite the sequence surrounding Ser296 (FSKHIQS296NL) being only weakly related to the optimal Chk1-recognition motif (M/I/L/V)-X-(R/K)-X-X-(S/T), where (S/T) is the phosphorylated residue |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-217904 |
Ser296 |
GFSKHIQsNLDFSPV |
Homo sapiens |
U2-OS Cell |
pmid |
sentence |
23068608 |
TheSer296autophosphorylation ofCHK1is mainly regulated by an intramolecular mechanism in response to DNA damage. |
|
Publications: |
2 |
Organism: |
Xenopus Laevis, Homo Sapiens |
Pathways: | DNA repair in cancer, FLT3-ITD signaling, Cell cycle: G2/M phase transition |
+ |
ATM | up-regulates
phosphorylation
|
CHEK1 |
0.84 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-163106 |
Ser317 |
ENVKYSSsQPEPRTG |
Homo sapiens |
|
pmid |
sentence |
20068082 |
Atr (predominantly) or atm (to a lesser extent) phosphorylates chk1 at ser317/345, directly leading to activation. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-163110 |
Ser345 |
LVQGISFsQPTCPDH |
Homo sapiens |
|
pmid |
sentence |
20068082 |
Atr (predominantly) or atm (to a lesser extent) phosphorylates chk1 at ser317/345, directly leading to activation. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
Pathways: | DNA repair in cancer, FLT3-ITD signaling, Cell cycle: G2/M phase transition |
+ |
PPP2CB | down-regulates activity
dephosphorylation
|
CHEK1 |
0.269 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-248579 |
Ser317 |
ENVKYSSsQPEPRTG |
Homo sapiens |
|
pmid |
sentence |
17015476 |
Phosphorylation of Chk1 by ATR is antagonized by a Chk1-regulated protein phosphatase 2A circuit|In response to genotoxic stress, Chk1 is phosphorylated on serines 317 (S317) and 345 (S345) by the ataxia-telangiectasia-related (ATR) protein kinase. Phosphorylation of Chk1 on these C-terminal serine residues is used as an indicator of Chk1 activation in vivo. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-248578 |
Ser345 |
LVQGISFsQPTCPDH |
Homo sapiens |
|
pmid |
sentence |
17015476 |
Phosphorylation of Chk1 by ATR is antagonized by a Chk1-regulated protein phosphatase 2A circuit|In response to genotoxic stress, Chk1 is phosphorylated on serines 317 (S317) and 345 (S345) by the ataxia-telangiectasia-related (ATR) protein kinase. Phosphorylation of Chk1 on these C-terminal serine residues is used as an indicator of Chk1 activation in vivo. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
ATR | up-regulates
phosphorylation
|
CHEK1 |
0.923 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-134712 |
Ser317 |
ENVKYSSsQPEPRTG |
Homo sapiens |
|
pmid |
sentence |
15775976 |
Atr activation typically leads to chk1 phosphorylation and activation. In response to genotoxic stress, chk1 is phosphorylated on serines 317 (s317) and 345 (s345) by the ataxia-telangiectasia-related (atr) protein kinase. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-134716 |
Ser345 |
LVQGISFsQPTCPDH |
Homo sapiens |
|
pmid |
sentence |
15775976 |
Atr activation typically leads to chk1 phosphorylation and activation. In response to genotoxic stress, chk1 is phosphorylated on serines 317 (s317) and 345 (s345) by the ataxia-telangiectasia-related (atr) protein kinase. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
Pathways: | DNA repair in cancer, FLT3-ITD signaling, Cell cycle: G2/M phase transition |
+ |
PPM1F | down-regulates activity
dephosphorylation
|
CHEK1 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-276987 |
Ser317 |
ENVKYSSsQPEPRTG |
Homo sapiens |
|
pmid |
sentence |
31944151 |
As a result, inactivation of Chk1 by POPX2 leads to impaired G1S checkpoint activation and cells are able to proceed from G1 to S phase despite DNA damage.|We also determined that POPX2 can dephosphorylate Chk1Ser317 and -Ser345 and is a potential regulator of Chk1 function in the cell. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-276988 |
Ser345 |
LVQGISFsQPTCPDH |
Homo sapiens |
|
pmid |
sentence |
31944151 |
As a result, inactivation of Chk1 by POPX2 leads to impaired G1S checkpoint activation and cells are able to proceed from G1 to S phase despite DNA damage.|We also determined that POPX2 can dephosphorylate Chk1Ser317 and -Ser345 and is a potential regulator of Chk1 function in the cell. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
PPP2CA | down-regulates activity
dephosphorylation
|
CHEK1 |
0.474 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-248616 |
Ser317 |
ENVKYSSsQPEPRTG |
Homo sapiens |
|
pmid |
sentence |
17015476 |
Phosphorylation of Chk1 by ATR is antagonized by a Chk1-regulated protein phosphatase 2A circuit|In response to genotoxic stress, Chk1 is phosphorylated on serines 317 (S317) and 345 (S345) by the ataxia-telangiectasia-related (ATR) protein kinase. Phosphorylation of Chk1 on these C-terminal serine residues is used as an indicator of Chk1 activation in vivo. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-248615 |
Ser345 |
LVQGISFsQPTCPDH |
Homo sapiens |
|
pmid |
sentence |
17015476 |
Phosphorylation of Chk1 by ATR is antagonized by a Chk1-regulated protein phosphatase 2A circuit|In response to genotoxic stress, Chk1 is phosphorylated on serines 317 (S317) and 345 (S345) by the ataxia-telangiectasia-related (ATR) protein kinase. Phosphorylation of Chk1 on these C-terminal serine residues is used as an indicator of Chk1 activation in vivo. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
CHEK1 | down-regulates
phosphorylation
|
NFKB1 |
0.279 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-195208 |
Ser328 |
INITKPAsVFVQLRR |
Homo sapiens |
|
pmid |
sentence |
22152481 |
Taken together, the above findings suggest that chk1 phosphorylates p50 at s329 and further, that this phosphorylation blocks p50 dna binding. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CHEK1 | up-regulates activity
phosphorylation
|
FANCD2 |
0.604 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-263252 |
Ser331 |
KSKGRASsSGNQESS |
Homo sapiens |
Fanconi Anemia Disease Specific Cell Type |
pmid |
sentence |
19861535 |
In this study, we report a novel phosphorylation site serine 331 (S331) of FANCD2, the pivotal downstream player of the Fanconi anemia pathway. Phosphorylation of S331 is important for its DNA damage-inducible monoubiquitylation, resistance to DNA cross-linkers, and in vivo interaction with FANCD1/BRCA2.|In vitro and in vivo experiments show that phosphorylation of S331 is mediated by CHK1, |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-107042 |
Ser331 |
KSKGRASsSGNQESS |
Homo sapiens |
HeLa Cell |
pmid |
sentence |
19861535 |
In vitro and in vivo experiments show that phosphorylation of s331 is mediated by chk1, the s-phase checkpoint kinase implicated in the fanconi anemia dna repair pathway. phosphorylation at this site is dependent on chk1, signifying the importance of the s-phase checkpoint in the activation of fanconi anemia pathway. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
CHEK1 | up-regulates
phosphorylation
|
AURKB |
0.367 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-152926 |
Ser331 |
HPWVRANsRRVLPPS |
Homo sapiens |
|
pmid |
sentence |
17276342 |
Chk1 phosphorylates aurora-b and enhances its catalytic activity in vitro. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CHEK1 | down-regulates activity
phosphorylation
|
MDM4 |
0.536 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-250770 |
Ser342 |
SKLTHSLsTSDITAI |
Homo sapiens |
SAOS-2 Cell |
pmid |
sentence |
16163388 |
MDMX is a direct substrate for Chk1 and Chk2 in vitro. Phosphorylation of MDMX leads to increased binding to MDM2 and more efficient ubiquitination, providing an explanation for the enhanced degradation of MDMX after DNA damage. | Western blot showed that Chk1 modified S342 and S367, but with strong preference for S342. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
PPM1D | down-regulates
dephosphorylation
|
CHEK1 |
0.487 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-135972 |
Ser345 |
LVQGISFsQPTCPDH |
Homo sapiens |
|
pmid |
sentence |
15870257 |
Ppm1d dephosphorylates chk1 phospho-ser 345 |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
PPM1D | down-regulates activity
dephosphorylation
|
CHEK1 |
0.487 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-248317 |
Ser345 |
LVQGISFsQPTCPDH |
Homo sapiens |
|
pmid |
sentence |
15870257 |
Here we show that the oncogenic p53-induced serine/threonine phosphatase, PPM1D (or Wip1), dephosphorylates two ATM/ATR targets, Chk1 and p53. PPM1D binds Chk1 and dephosphorylates the ATR-targeted phospho-Ser 345, leading to decreased Chk1 kinase activity. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-276986 |
Ser345 |
LVQGISFsQPTCPDH |
Homo sapiens |
|
pmid |
sentence |
18265945 |
Because Chk1 phosphorylates and activates p53, the inhibition of Chk1 by Wip1 also places Wip1 in a negative feedback regulatory loop for p53 .|In vitro phosphatase assays showed that Wip1 dephosphorylated Chk1 at Ser345, but not Ser317. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
CHEK1 | down-regulates quantity by destabilization
phosphorylation
|
MDM4 |
0.536 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-178067 |
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 |
+ |
CHEK1 | down-regulates activity
phosphorylation
|
PABIR1 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-266380 |
Ser37 |
GGLRRSNsAPLIHGL |
Homo sapiens |
A-549 Cell |
pmid |
sentence |
33108758 |
Knockout of FAM122A results in activation of PP2A-B55α, a phosphatase that dephosphorylates the WEE1 protein and rescues WEE1 from ubiquitin-mediated degradation. in tumor cells with oncogene-driven replication stress, CHK1 can directly phosphorylate FAM122A, leading to activation of the PP2A-B55α phosphatase and increased WEE1 expression. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CHEK1 | up-regulates
phosphorylation
|
FANCE |
0.705 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-153023 |
Ser374 |
LFLGRILsLTSSASR |
Homo sapiens |
|
pmid |
sentence |
17296736 |
Chk1 directly phosphorylates the fance subunit of the fa core complex on two conserved sites (threonine 346 and serine 374). chk1-mediated phosphorylation of fance is required for the fanconi anemia/brca pathway. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-153027 |
Thr346 |
LGLLRLCtWLLALSP |
Homo sapiens |
|
pmid |
sentence |
17296736 |
Chk1 directly phosphorylates the fance subunit of the fa core complex on two conserved sites (threonine 346 and serine 374). chk1-mediated phosphorylation of fance is required for the fanconi anemia/brca pathway. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
CHEK1 | up-regulates
phosphorylation
|
TP73 |
0.517 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-118913 |
Ser47 |
EVVGGTDsSMDVFHL |
Homo sapiens |
|
pmid |
sentence |
14585975 |
We found that endogenous p73alpha is serine phosphorylated by endogenous chk1 upon dna damage, which is a mechanism required for the apoptotic-inducing function of p73alpha. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CHEK1 | down-regulates activity
phosphorylation
|
SETMAR |
0.504 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-273610 |
Ser508 |
LYDNRRRsAQWLDQE |
Homo sapiens |
HEK-293 Cell |
pmid |
sentence |
25024738 |
We previously found that Chk1 phosphorylation of Metnase on S495 enhanced its DNA DSB repair activity but decreased its ability to re-start stalled replication forks. Here we show that phosphorylated Metnase feeds back to increase the half-life of Chk1. Chk1 half-life is regulated by DDB1 targeting it to Cul4A for ubiquitination and destruction. Metnase decreases Chk1 interaction with DDB1, and decreases Chk1 ubiquitination. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CHEK1 | up-regulates activity
phosphorylation
|
RB1 |
0.432 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-153904 |
Ser612 |
MYLSPVRsPKKKGST |
Homo sapiens |
|
pmid |
sentence |
17380128 |
These results suggest that ser612 is phosphorylated by chk1/2 after dna damage, leading to the formation of prb-e2f-1. 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: G2/M phase transition |
+ |
CHEK1 | up-regulates
phosphorylation
|
BLM |
0.772 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-167534 |
Ser646 |
LKHERFQsLSFPHTK |
Homo sapiens |
|
pmid |
sentence |
20719863 |
Hese results indicated that chk1-mediated phosphorylation on blm at ser(646) might be a determinant for regulating subnuclear localization and could act as a marker for the activation status of blm in response to dna damage. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CHEK1 | down-regulates
phosphorylation
|
TLK1 |
0.442 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-99653 |
Ser743 |
PHMRRSNsSGNLHMA |
Homo sapiens |
|
pmid |
sentence |
12660173 |
Chk1 phosphorylates tlk1 on serine 695 (s695) these findings identify an unprecedented functional co- operation between atm and chk1 in propagation of a checkpoint response during s phase and suggest that, through transient inhibition of tlk kinases, the atm_chk1_tlk pathway may regulate processes involved in chromatin assembly. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CHEK1 | down-regulates activity
phosphorylation
|
TLK2 |
0.273 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-262740 |
Ser750 |
PHIRKSVsTSSPAGA |
in vitro |
|
pmid |
sentence |
12955071 |
Chk1 phosphorylates GST-fusion fragments of TLK1 in vitro.When Chk1 protein was depleted in cells transfected with pSuper-Chk1, TLK activity was not suppressed after short aphidicolin treatment of S-phase cells (Figure 8a, b). |
|
Publications: |
1 |
Organism: |
In Vitro |
+ |
CHEK1 | down-regulates activity
phosphorylation
|
H3-3A |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-160557 |
Thr12 |
KQTARKStGGKAPRK |
Homo sapiens |
|
pmid |
sentence |
18243098 |
We identify chk1 as the kinase responsible for h3-t11 phosphorylation. H3-t11 phosphorylation occurs throughout the cell cycle and is chk1 dependent in vivo.Phosphorylation at thr-12 (h3t11ph) by pkn1 is a specific tag for epigenetic transcriptional activation that promotes demethylation of lys-10 (h3k9me) by kdm4c/jmjd2c. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CHEK1 | down-regulates quantity by destabilization
phosphorylation
|
BLM |
0.772 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-276909 |
Thr182 |
SHFVRVStAQKSKKG |
Homo sapiens |
HEK-293T Cell |
pmid |
sentence |
26028025 |
We now provide evidence that BLM undergoes K48-linked ubiquitylation and subsequent degradation during mitosis due to the E3 ligase, Fbw7α. Fbw7α carries out its function after GSK3β- and CDK2/cyclin A2-dependent phosphorylation events on Thr171 and Ser175 of BLM which lies within a well-defined phosphodegron, a sequence which is conserved in all primates.Phosphorylation on BLM Thr171 and Ser175 depends on prior phosphorylation at Thr182 by Chk1/Chk2. Thr182 phosphorylation not only controls BLM ubiquitylation and degradation during mitosis but is also a determinant for its localization on the ultrafine bridges. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CHEK1 | up-regulates
phosphorylation
|
RAD51 |
0.837 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-133375 |
Thr309 |
LRKGRGEtRICKIYD |
Homo sapiens |
|
pmid |
sentence |
15665856 |
We demonstrate that chk1 interacts with rad51, and that rad51 is phosphorylated on thr 309 in a chk1-dependent manner |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | DNA repair in cancer, FLT3-ITD signaling, Cell cycle: G2/M phase transition |
+ |
CHEK1 | up-regulates
phosphorylation
|
CLSPN |
0.786 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-149411 |
Thr916 |
DELLDLCtGKFTSQA |
Homo sapiens |
|
pmid |
sentence |
16963448 |
We found that thr-916 on claspin is phosphorylated by chk1, suggesting that chk1 regulates claspin during checkpoint response. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CHEK1 |
phosphorylation
|
SNCB |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-174590 |
Tyr127 |
EDPPQEEyQEYEPEA |
Homo sapiens |
|
pmid |
sentence |
21699177 |
Chk preferentially phosphorylates recombinant _-synuclein at tyrosine-127 |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CHIR-124 | down-regulates
chemical inhibition
|
CHEK1 |
0.8 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-190973 |
|
|
Homo sapiens |
|
pmid |
sentence |
Other |
|
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
SCHEMBL14517914 | down-regulates
chemical inhibition
|
CHEK1 |
0.8 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-163231 |
|
|
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 |
+ |
MUTYH | up-regulates
|
CHEK1 |
0.349 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-173969 |
|
|
Homo sapiens |
|
pmid |
sentence |
21615992 |
Hmyh is involved in the activation mechanism of chk1 upon dna damage, but not in stability or inactivation. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CHEK1 | down-regulates activity
|
MEK1/2 |
0.329 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-263059 |
|
|
Homo sapiens |
|
pmid |
sentence |
28138032 |
Mechanistically, Ras-MEK signaling drives Chk1 expression and promotes cancer cell growth that produces genotoxic stress that requires Chk1 to mediate a response to the consequent DNA damage. Reciprocally, Chk1 engages a negative feedback loop to prevent hyperactivation of Ras-MEK signaling, thereby limiting DNA damage. Ras–MEK signaling transcriptionally activates Chk1, which appears to sustain cancer cell growth by maintaining DNA damage levels below a threshold that would otherwise drive apoptosis. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | FLT3-ITD signaling |
+ |
MEK1/2 | up-regulates quantity by expression
transcriptional regulation
|
CHEK1 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-263069 |
|
|
Homo sapiens |
|
pmid |
sentence |
28138032 |
Mechanistically, Ras-MEK signaling drives Chk1 expression and promotes cancer cell growth that produces genotoxic stress that requires Chk1 to mediate a response to the consequent DNA damage. Reciprocally, Chk1 engages a negative feedback loop to prevent hyperactivation of Ras-MEK signaling, thereby limiting DNA damage. Ras–MEK signaling transcriptionally activates Chk1, which appears to sustain cancer cell growth by maintaining DNA damage levels below a threshold that would otherwise drive apoptosis. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | FLT3-ITD signaling |
+ |
6-bromo-3-(1-methyl-4-pyrazolyl)-5-(3-piperidinyl)-7-pyrazolo[1,5-a]pyrimidinamine | down-regulates
chemical inhibition
|
CHEK1 |
0.8 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-206838 |
|
|
Homo sapiens |
|
pmid |
sentence |
Other |
|
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
GSK3B | down-regulates activity
|
CHEK1 |
0.302 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-263050 |
|
|
Mus musculus |
|
pmid |
sentence |
24260231 |
Involvement of GSK3 Inhibition by the PI3K/Akt Pathway in Regulation of Etoposide-induced Chk1 Activation. GSK3ß regulates etoposide-induced Chk1 activation. GSK3 inhibitors, including LiCl and SB216763, restored the sustained Chk1 activation and mitigated apoptosis in cells treated with etoposide and the inhibitors for aberrant kinases, PI3K, or Akt. Thus, proteasomal degradation of Chk1 as well as GSK3 activation may be involved in negative regulation of etoposide-induced Chk1 by imatinib in these cells. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
Pathways: | FLT3-ITD signaling, Cell cycle: G2/M phase transition |
+ |
LY2603618 | down-regulates activity
chemical inhibition
|
CHEK1 |
0.8 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-262538 |
|
|
Homo sapiens |
|
pmid |
sentence |
33261142 |
Here, using a panel of basal-like cancer cell lines, we explored the synergistic interactions of CHK1 inhibitors (rabusertib and SAR020106) with approved therapies in breast cancer and evaluated their potential to overcome resistance. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | FLT3-ITD signaling |
+ |
3-(carbamoylamino)-5-(3-fluorophenyl)-N-[(3S)-3-piperidinyl]-2-thiophenecarboxamide | down-regulates
chemical inhibition
|
CHEK1 |
0.8 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-190203 |
|
|
Homo sapiens |
|
pmid |
sentence |
Other |
|
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
1-[5-bromo-4-methyl-2-[[(2S)-2-morpholinyl]methoxy]phenyl]-3-(5-methyl-2-pyrazinyl)urea | down-regulates
chemical inhibition
|
CHEK1 |
0.8 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-193787 |
|
|
Homo sapiens |
|
pmid |
sentence |
Other |
|
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
FBXO6 | down-regulates quantity by destabilization
binding
|
CHEK1 |
0.511 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-271879 |
|
|
Homo sapiens |
HEK-293 Cell |
pmid |
sentence |
19716789 |
Here, we report that DNA damage not only activates Chk1, but also exposes a degron-like region at the carboxyl terminus of Chk1 to an Fbx6-containing SCF (Skp1-Cul1-F box) E3 ligase, which mediates the ubiquitination and degradation of Chk1 and, in turn, terminates the checkpoint. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
DNA_damage | up-regulates
|
CHEK1 |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-242616 |
|
|
Homo sapiens |
|
pmid |
sentence |
26527132 |
Checkpoint kinase 1 (CHK1) is a key component of the ATR-dependent DNA damage response pathway that protects cells from RS by preventing replication fork collapse and activating homologous DNA repair. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | DNA repair in cancer, FLT3-ITD signaling, Cell cycle: G2/M phase transition |
+ |
7-Hydroxystaurosporine | down-regulates
chemical inhibition
|
CHEK1 |
0.8 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-163222 |
|
|
Homo sapiens |
|
pmid |
sentence |
20068082 |
The clinical use of ucn-01, the first chk1 inhibitor evaluated in humans, is limited by its prolonged plasma half-life due to extensive plasma binding to alfa1 acidic glycoprotein |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CHEK1 | down-regulates activity
phosphorylation
|
Histone H3 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-265326 |
|
|
Homo sapiens |
|
pmid |
sentence |
18243098 |
We identify chk1 as the kinase responsible for h3-t11 phosphorylation. H3-t11 phosphorylation occurs throughout the cell cycle and is chk1 dependent in vivo.Phosphorylation at thr-12 (h3t11ph) by pkn1 is a specific tag for epigenetic transcriptional activation that promotes demethylation of lys-10 (h3k9me) by kdm4c/jmjd2c. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CHEK1 | up-regulates
phosphorylation
|
CDC7 |
0.724 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-163161 |
|
|
Homo sapiens |
|
pmid |
sentence |
20068082 |
Chk1 directly phosphorylates essential s-phase kinases cdc7. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
TIMELESS | up-regulates activity
binding
|
CHEK1 |
0.788 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-268054 |
|
|
Chlorocebus aethiops |
|
pmid |
sentence |
23418588 |
We performed a detailed molecular characterization of TIM interactions with the core clock protein CRY1 and the DNA damage signal transducer CHK1, and found that the N-terminus of TIM is required for association with both proteins, as well as for homodimerization. |
|
Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
+ |
Cullin 1-RBX1-Skp1 | down-regulates quantity by destabilization
polyubiquitination
|
CHEK1 |
0.458 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-271880 |
|
|
Homo sapiens |
HEK-293 Cell |
pmid |
sentence |
19716789 |
Here, we report that DNA damage not only activates Chk1, but also exposes a degron-like region at the carboxyl terminus of Chk1 to an Fbx6-containing SCF (Skp1-Cul1-F box) E3 ligase, which mediates the ubiquitination and degradation of Chk1 and, in turn, terminates the checkpoint. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CHEK1 | up-regulates
phosphorylation
|
WEE1 |
0.595 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-163164 |
|
|
Homo sapiens |
|
pmid |
sentence |
20068082 |
Chk1 also phosphorylates and stabilizes wee1. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CLSPN | up-regulates
binding
|
CHEK1 |
0.786 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-84474 |
|
|
Homo sapiens |
|
pmid |
sentence |
11090622 |
Binding of claspin to xchk1 is highly elevated in the presence of dna templates that trigger a checkpoint arrest of the cell cycle in xenopus egg extracts |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
SETMAR | up-regulates quantity by stabilization
|
CHEK1 |
0.504 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-273609 |
|
|
Homo sapiens |
HEK-293 Cell |
pmid |
sentence |
25024738 |
We previously found that Chk1 phosphorylation of Metnase on S495 enhanced its DNA DSB repair activity but decreased its ability to re-start stalled replication forks. Here we show that phosphorylated Metnase feeds back to increase the half-life of Chk1. Chk1 half-life is regulated by DDB1 targeting it to Cul4A for ubiquitination and destruction. Metnase decreases Chk1 interaction with DDB1, and decreases Chk1 ubiquitination. Phosphorylated Chk1 phosphorylates S495 of Metnase. Phosphorylated Metnase decreases the interaction of DDB1 with Chk1, reducing Chk1 targeting to the Cul4a E3 ubiquitin ligase, increasing Chk1 stability. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |