+ |
CHEK2 | up-regulates quantity by stabilization
phosphorylation
|
AATF |
0.365 |
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 |
+ |
ATM | up-regulates quantity by stabilization
phosphorylation
|
AATF |
0.362 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-264415 |
Ser189 |
EGDDAEDsQGESEED |
Homo sapiens |
HCT-116 Cell |
pmid |
sentence |
17157788 |
The checkpoint kinases ATM/ATR and Chk2 interact with Che-1 and promote its phosphorylation and accumulation in response to DNA damage. These Che-1 modifications induce a specific recruitment of Che-1 on the TP53 and p21 promoters. |DNA damage stabilizes Che-1 protein|In addition, substitution of Che-1 Ser187 with an alanine (Che-1S187A) prevented Che-1 phosphorylation by ATM (Figure 2F), supporting this residue as an ATM-target site. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MAPKAPK2 | up-regulates
phosphorylation
|
AATF |
0.332 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-191935 |
Thr366 |
FTVYRNRtLQKWHDK |
Homo sapiens |
|
pmid |
sentence |
22909821 |
Upon genotoxic stress, aatf is phosphorylated by the checkpoint kinase mk2. Phosphorylation results in the release of aatf from cytoplasmic mrlc3 and subsequent nuclear translocation where aatf binds to the puma, bax and bak promoter regions to repress p53-driven expression of these pro-apoptotic genes. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
AATF | down-regulates quantity
transcriptional regulation
|
BAX |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-259916 |
|
|
Homo sapiens |
|
pmid |
sentence |
22909821 |
We identify the transcriptional regulator apoptosis-antagonizing transcription factor (AATF)/Che-1 as a critical regulator of the cellular outcome of the p53 response. Upon genotoxic stress, AATF is phosphorylated by the checkpoint kinase MK2. Phosphorylation results in the release of AATF from cytoplasmic MRLC3 and subsequent nuclear translocation where AATF binds to the PUMA, BAX and BAK promoter regions to repress p53-driven expression of these pro-apoptotic genes. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
AATF | up-regulates quantity by expression
transcriptional regulation
|
KLK3 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-253669 |
|
|
|
|
pmid |
sentence |
23146908 |
Chromatin immunoprecipitation in combination with siRNA-mediated knockdown revealed that recruitment of AATF and ZIPK to the PSA enhancer was dependent on AR, whereas recruitment of TSG101 was dependent on AATF. |
|
Publications: |
1 |