| + |
CASP3 | down-regulates quantity by destabilization 
cleavage
|
BRCA1 |
0.463 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256326 |
Asp1155 |
ETPDDLLdDGEIKED |
Homo sapiens |
|
| pmid |
sentence |
| 12149654 |
We demonstrate the cleavage and the consequential downregulation of full-length BRCA1 by caspase-3 during UV-induced apoptosis. Finally, mutation of a caspase-3 specific cleavage site (D/A1154) rendered BRCA1 non-cleavable. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
Caspase 3 complex | down-regulates quantity by destabilization
cleavage
|
BRCA1 |
0.463 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256432 |
Asp1155 |
ETPDDLLdDGEIKED |
Homo sapiens |
|
| pmid |
sentence |
| 12149654 |
We demonstrate the cleavage and the consequential downregulation of full-length BRCA1 by caspase-3 during UV-induced apoptosis. Finally, mutation of a caspase-3 specific cleavage site (D/A1154) rendered BRCA1 non-cleavable. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
BRCA1 | up-regulates activity 
ubiquitination
|
MACROH2A1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-278752 |
Lys123 |
KKRGSKGkLEAIITP |
Homo sapiens |
|
| pmid |
sentence |
| 28564596 |
BRCA1 Ubiquitinates K123 of mH2A1 in a Ligase-Activity-Dependent Manner. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
BRCA1 | down-regulates quantity by destabilization
ubiquitination
|
NSD2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-278745 |
Lys292 |
EGEGQFEkLCQESAK |
Homo sapiens |
|
| pmid |
sentence |
| 32826945 |
Proteomic data analysis revealed interaction between NSD2 and BRCA1 and further study revealed that BRCA1 ubiquitinates NSD2 at K292 residue.|These results suggested that BRCA1 interacts with and promotes degradation of NSD2 via polyubiquitination . |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATR | up-regulates activity
phosphorylation
|
BRCA1 |
0.808 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250581 |
Ser1143 |
PMGSSHAsQVCSETP |
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 11114888 |
Of the four potential phosphoacceptor sites in the BRCA1 (1005–1313) fragment (Ser 1143, Ser 1239, Ser 1280, Ser 1298), Ala substitutions at two sites, Ser 1143 and Ser 1280, reduced the in vitro phosphorylation of GST–BRCA1 (1005–1313) by ATR, whereas substitution of Ser 1239 or Ser 1298 with Ala had little or no effect (Fig. 2C; data not shown). A Ser 1143/Ser 1280 double mutant was a poor substrate for ATR, suggesting that these are the two major in vitro phosphorylation sites on this BRCA1 fragment. | Together, these results demonstrate that ATR and BRCA1 are components of the same genotoxic stress-responsive pathway, and that ATR directly phosphorylates BRCA1 in response to damaged DNA or stalled DNA replication. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250582 |
Ser1280 |
QVILAKAsQEHHLSE |
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 11114888 |
Of the four potential phosphoacceptor sites in the BRCA1 (1005–1313) fragment (Ser 1143, Ser 1239, Ser 1280, Ser 1298), Ala substitutions at two sites, Ser 1143 and Ser 1280, reduced the in vitro phosphorylation of GST–BRCA1 (1005–1313) by ATR, whereas substitution of Ser 1239 or Ser 1298 with Ala had little or no effect (Fig. 2C; data not shown). A Ser 1143/Ser 1280 double mutant was a poor substrate for ATR, suggesting that these are the two major in vitro phosphorylation sites on this BRCA1 fragment. | Together, these results demonstrate that ATR and BRCA1 are components of the same genotoxic stress-responsive pathway, and that ATR directly phosphorylates BRCA1 in response to damaged DNA or stalled DNA replication. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-106432 |
Ser1387 |
EDCSGLSsQSDILTT |
Homo sapiens |
Lymphoblastoid Cell Line |
| pmid |
sentence |
| 11278964 |
Brca1 is phosphorylated at ser-1423 and ser-1524 after ir and uv;however, ser-1387 is specifically phosphorylated after ir, and ser-1457 is predominantly phosphorylated after uv.atr controls brca1 phosphorylation in vivo. Taken together, our results support a model in which atm and atr act in parallel but somewhat overlapping pathways of dna damage signaling but respond primarily to different types of dna lesion. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-106436 |
Ser1423 |
AVLEQHGsQPSNSYP |
Homo sapiens |
Lymphoblastoid Cell Line |
| pmid |
sentence |
| 11278964 |
Brca1 is phosphorylated at ser-1423 and ser-1524 after ir and uv;however, ser-1387 is specifically phosphorylated after ir, and ser-1457 is predominantly phosphorylated after uv.atr controls brca1 phosphorylation in vivo. Taken together, our results support a model in which atm and atr act in parallel but somewhat overlapping pathways of dna damage signaling but respond primarily to different types of dna lesion. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-106440 |
Ser1457 |
SEKAVLTsQKSSEYP |
Homo sapiens |
Lymphoblastoid Cell Line |
| pmid |
sentence |
| 11278964 |
Brca1 is phosphorylated at ser-1423 and ser-1524 after ir and uv;however, ser-1387 is specifically phosphorylated after ir, and ser-1457 is predominantly phosphorylated after uv.atr controls brca1 phosphorylation in vivo. Taken together, our results support a model in which atm and atr act in parallel but somewhat overlapping pathways of dna damage signaling but respond primarily to different types of dna lesion. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250583 |
Thr1394 |
SQSDILTtQQRDTMQ |
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 11114888 |
Although no single mutation eliminated the GST–BRCA1 (1314–1863) electrophoretic mobility shift, a quadruple mutant (GST–BRCA14A) containing Ala substitutions at Ser 1387, Thr 1394, Ser 1423, and Ser 1457 showed no alteration in electrophoretic mobility after phosphorylation by ATR-containing immune complexes (Fig.2D). The total incorporation of 32Pi into the GST–BRCA14Asubstrate was reduced by 70% relative to that obtained with wild-type GST–BRCA1 (1314–1863), suggesting that these four residues account for most, but not all of the phosphorylation sites in this fragment. | Together, these results demonstrate that ATR and BRCA1 are components of the same genotoxic stress-responsive pathway, and that ATR directly phosphorylates BRCA1 in response to damaged DNA or stalled DNA replication. |
|
| Publications: |
6 |
Organism: |
Homo Sapiens |
| Pathways: | DNA repair in cancer, Cell cycle: G2/M phase transition |
| + |
CDK1 | up-regulates
phosphorylation
|
BRCA1 |
0.487 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-72083 |
Ser1189 |
QKGELSRsPSPFTHT |
Homo sapiens |
Breast Cancer Cell |
| pmid |
sentence |
| 10550055 |
However, shrna-mediated depletion of cdk1 alone or small molecule cdk1 inhibition abrogated s phase cell-cycle arrest and the phosphorylation of a subset of atr/atm targets after dna damage. Loss of dna damage-induced checkpoint control was caused by a reduction in formation of brca1-containing foci. Mutation of brca1 at s1497 and s1189/s1191 resulted in loss of cdk1-mediated phosphorylation and also compromised formation of brca1-containing foci. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-187595 |
Ser1189 |
QKGELSRsPSPFTHT |
Homo sapiens |
Lung Cancer Cell |
| pmid |
sentence |
| 19683496 |
However, shrna-mediated depletion of cdk1 alone or small molecule cdk1 inhibition abrogated s phase cell-cycle arrest and the phosphorylation of a subset of atr/atm targets after dna damage. Loss of dna damage-induced checkpoint control was caused by a reduction in formation of brca1-containing foci. Mutation of brca1 at s1497 and s1189/s1191 resulted in loss of cdk1-mediated phosphorylation and also compromised formation of brca1-containing foci. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-187599 |
Ser1191 |
GELSRSPsPFTHTHL |
Homo sapiens |
Lung Cancer Cell |
| pmid |
sentence |
| 19683496 |
However, shrna-mediated depletion of cdk1 alone or small molecule cdk1 inhibition abrogated s phase cell-cycle arrest and the phosphorylation of a subset of atr/atm targets after dna damage. Loss of dna damage-induced checkpoint control was caused by a reduction in formation of brca1-containing foci. Mutation of brca1 at s1497 and s1189/s1191 resulted in loss of cdk1-mediated phosphorylation and also compromised formation of brca1-containing foci. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-187603 |
Ser1497 |
EPGVERSsPSKCPSL |
Homo sapiens |
Lung Cancer Cell |
| pmid |
sentence |
| 19683496 |
However, shrna-mediated depletion of cdk1 alone or small molecule cdk1 inhibition abrogated s phase cell-cycle arrest and the phosphorylation of a subset of atr/atm targets after dna damage. Loss of dna damage-induced checkpoint control was caused by a reduction in formation of brca1-containing foci. Mutation of brca1 at s1497 and s1189/s1191 resulted in loss of cdk1-mediated phosphorylation and also compromised formation of brca1-containing foci. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-72087 |
Ser1497 |
EPGVERSsPSKCPSL |
Homo sapiens |
Breast Cancer Cell |
| pmid |
sentence |
| 10550055 |
However, shrna-mediated depletion of cdk1 alone or small molecule cdk1 inhibition abrogated s phase cell-cycle arrest and the phosphorylation of a subset of atr/atm targets after dna damage. Loss of dna damage-induced checkpoint control was caused by a reduction in formation of brca1-containing foci. Mutation of brca1 at s1497 and s1189/s1191 resulted in loss of cdk1-mediated phosphorylation and also compromised formation of brca1-containing foci. |
|
| Publications: |
5 |
Organism: |
Homo Sapiens |
| + |
ATM | up-regulates
phosphorylation
|
BRCA1 |
0.829 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-72048 |
Ser1330 |
QMRHQSEsQGVGLSD |
Homo sapiens |
Breast Cancer Cell |
| pmid |
sentence |
| 10550055 |
The brca1 (breast cancer gene 1) tumor suppressor protein is phosphorylated in response to dna damage. phosphorylation of brca1 by the checkpoint kinase atm may be critical for proper responses to dna double-strand breaks |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-91482 |
Ser1387 |
EDCSGLSsQSDILTT |
Homo sapiens |
Breast Cancer Cell |
| pmid |
sentence |
| 12183412 |
Phosphorylation of serine 1387 in brca1 is specifically required for the atm-mediated s-phase checkpoint after ionizing irradiation.We recently reported that brca1 function is required for appropriate cell cycle arrests after ionizing irradiation in both the s-phase and the g2 phase of the cell cycle. We also found that mutation of serine 1423 in brca1, a target of atm phosphorylation, abrogates the g2-m checkpoint but not the ionizing irradiation-induced s-phase checkpoint. Here we demonstrate that mutation of serine 1387 in brca1, another target of atm phosphorylation, conversely abrogates the radiation-induced s-phase arrest but does not affect the g2-m checkpoint. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-72052 |
Ser1423 |
AVLEQHGsQPSNSYP |
Homo sapiens |
Breast Cancer Cell |
| pmid |
sentence |
| 10550055 |
Phosphorylation of serine 1387 in brca1 is specifically required for the atm-mediated s-phase checkpoint after ionizing irradiation.We recently reported that brca1 function is required for appropriate cell cycle arrests after ionizing irradiation in both the s-phase and the g2 phase of the cell cycle. We also found that mutation of serine 1423 in brca1, a target of atm phosphorylation, abrogates the g2-m checkpoint but not the ionizing irradiation-induced s-phase checkpoint. Here we demonstrate that mutation of serine 1387 in brca1, another target of atm phosphorylation, conversely abrogates the radiation-induced s-phase arrest but does not affect the g2-m checkpoint. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-72056 |
Ser1457 |
SEKAVLTsQKSSEYP |
Homo sapiens |
Breast Cancer Cell |
| pmid |
sentence |
| 10550055 |
The brca1 (breast cancer gene 1) tumor suppressor protein is phosphorylated in response to dna damage. phosphorylation of brca1 by the checkpoint kinase atm may be critical for proper responses to dna double-strand breaks |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-72060 |
Ser1466 |
KSSEYPIsQNPEGLS |
Homo sapiens |
Breast Cancer Cell |
| pmid |
sentence |
| 10550055 |
The brca1 (breast cancer gene 1) tumor suppressor protein is phosphorylated in response to dna damage. phosphorylation of brca1 by the checkpoint kinase atm may be critical for proper responses to dna double-strand breaks |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-187591 |
Ser1497 |
EPGVERSsPSKCPSL |
Homo sapiens |
Lung Cancer Cell |
| pmid |
sentence |
| 19683496 |
However, shrna-mediated depletion of cdk1 alone or small molecule cdk1 inhibition abrogated s phase cell-cycle arrest and the phosphorylation of a subset of atr/atm targets after dna damage. Loss of dna damage-induced checkpoint control was caused by a reduction in formation of brca1-containing foci. Mutation of brca1 at s1497 and s1189/s1191 resulted in loss of cdk1-mediated phosphorylation and also compromised formation of brca1-containing foci. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-72064 |
Ser1497 |
EPGVERSsPSKCPSL |
Homo sapiens |
Breast Cancer Cell |
| pmid |
sentence |
| 10550055 |
However, shrna-mediated depletion of cdk1 alone or small molecule cdk1 inhibition abrogated s phase cell-cycle arrest and the phosphorylation of a subset of atr/atm targets after dna damage. Loss of dna damage-induced checkpoint control was caused by a reduction in formation of brca1-containing foci. Mutation of brca1 at s1497 and s1189/s1191 resulted in loss of cdk1-mediated phosphorylation and also compromised formation of brca1-containing foci. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-72068 |
Ser1524 |
LQNRNYPsQEELIKV |
Homo sapiens |
Breast Cancer Cell |
| pmid |
sentence |
| 10550055 |
The brca1 (breast cancer gene 1) tumor suppressor protein is phosphorylated in response to dna damage. phosphorylation of brca1 by the checkpoint kinase atm may be critical for proper responses to dna double-strand breaks. Phosphorylation of brca1 on ser1423 and ser1524 by atm |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-72072 |
Ser1542 |
EEQQLEEsGPHDLTE |
Homo sapiens |
Breast Cancer Cell |
| pmid |
sentence |
| 10550055 |
The brca1 (breast cancer gene 1) tumor suppressor protein is phosphorylated in response to dna damage. phosphorylation of brca1 by the checkpoint kinase atm may be critical for proper responses to dna double-strand breaks. Phosphorylation of brca1 on ser1423 and ser1524 by atm |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-72075 |
|
|
Homo sapiens |
Breast Cancer Cell |
| pmid |
sentence |
| 10550055 |
Results from this study indicate that the checkpoint protein kinase atm (mutated in ataxia telangiectasia) was required for phosphorylation of brca1 in response to ionizing radiation. Brca1 is phosphorylated at tyrosine residues in an atm-dependent, radiation-dependent manner. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-87845 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12024016 |
Results from this study indicate that the checkpoint protein kinase atm (mutated in ataxia telangiectasia) was required for phosphorylation of brca1 in response to ionizing radiation. Brca1 is phosphorylated at tyrosine residues in an atm-dependent, radiation-dependent manner. |
|
| Publications: |
11 |
Organism: |
Homo Sapiens |
| Pathways: | DNA repair in cancer, Cell cycle: G2/M phase transition |
| + |
PPP1CA | down-regulates activity
dephosphorylation
|
BRCA1 |
0.368 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-248561 |
Ser1423 |
AVLEQHGsQPSNSYP |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 17603999 |
Protein kinases involved in the DNA damage checkpoint control, such as ATM, ATR, and hCds1/Chk2, have been shown to phosphorylate and activate BRCA1 upon DNA damage. |Altogether, these results indicate that PP1α specifically dephosphorylates BRCA1 at multiple serine sites, including S988 [12], S1423, and S1524. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-248562 |
Ser1524 |
LQNRNYPsQEELIKV |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 17603999 |
Protein kinases involved in the DNA damage checkpoint control, such as ATM, ATR, and hCds1/Chk2, have been shown to phosphorylate and activate BRCA1 upon DNA damage. |Altogether, these results indicate that PP1α specifically dephosphorylates BRCA1 at multiple serine sites, including S988 [12], S1423, and S1524. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-248560 |
Ser988 |
PPLFPIKsFVKTKCK |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 17603999 |
Protein kinases involved in the DNA damage checkpoint control, such as ATM, ATR, and hCds1/Chk2, have been shown to phosphorylate and activate BRCA1 upon DNA damage. |Altogether, these results indicate that PP1α specifically dephosphorylates BRCA1 at multiple serine sites, including S988 [12], S1423, and S1524. |
|
| Publications: |
3 |
Organism: |
Homo Sapiens |
| + |
CDK2 | up-regulates
phosphorylation
|
BRCA1 |
0.691 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-72091 |
Ser1497 |
EPGVERSsPSKCPSL |
Homo sapiens |
|
| pmid |
sentence |
| 10550055 |
However, shrna-mediated depletion of cdk1 alone or small molecule cdk1 inhibition abrogated s phase cell-cycle arrest and the phosphorylation of a subset of atr/atm targets after dna damage. Loss of dna damage-induced checkpoint control was caused by a reduction in formation of brca1-containing foci. Mutation of brca1 at s1497 and s1189/s1191 resulted in loss of cdk1-mediated phosphorylation and also compromised formation of brca1-containing foci. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-187607 |
Ser1497 |
EPGVERSsPSKCPSL |
Homo sapiens |
Lung Cancer Cell |
| pmid |
sentence |
| 19683496 |
However, shrna-mediated depletion of cdk1 alone or small molecule cdk1 inhibition abrogated s phase cell-cycle arrest and the phosphorylation of a subset of atr/atm targets after dna damage. Loss of dna damage-induced checkpoint control was caused by a reduction in formation of brca1-containing foci. Mutation of brca1 at s1497 and s1189/s1191 resulted in loss of cdk1-mediated phosphorylation and also compromised formation of brca1-containing foci. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
ATM |
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4.0
BRCA1
- 
- 