| + |
DNA_damage | up-regulates 
|
TTK |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-242619 |
|
|
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 |
| + |
DNA_damage | up-regulates
|
ERCC8 |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-275690 |
|
|
|
|
| pmid |
sentence |
| 24086043 |
TC-NER is initiated by RNA polymerase stalled at a lesion with the help of TC-NER specific factors CSA, CSB, and XAB2. |
|
| Publications: |
1 |
| + |
DNA_damage | up-regulates quantity
|
TP53 |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-209690 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19879762 |
In the case of DNA-damage, phosphorylation of both p53 and Mdm2 by the checkpoint kinases ATM, ATR, Chk1 and Chk2 contributes to the dissociation of the Mdm2-p53 complex, leading to enhanced cellular p53 levels that primarily accumulate in the nucleus. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Colorectal Carcinoma, FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, Mitochondrial Control of Apoptosis, Non-small-cell lung cancer (NSCLC), P38 Signaling, p53 in cancer |
| + |
DNA_damage | up-regulates
|
ERCC6 |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-275691 |
|
|
|
|
| pmid |
sentence |
| 24086043 |
TC-NER is initiated by RNA polymerase stalled at a lesion with the help of TC-NER specific factors CSA, CSB, and XAB2. |
|
| Publications: |
1 |
| + |
DNA_damage | up-regulates
|
ATM |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-242612 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21034966 |
the ATM-Chk2 and ATR-Chk1 pathways, which are activated by DNA double-strand breaks (DSBs) and single-stranded DNA respectively. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Colorectal Carcinoma, DNA repair in cancer, FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer |
| + |
DNA_damage | up-regulates
|
ATR |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-242609 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21034966 |
the ATM-Chk2 and ATR-Chk1 pathways, which are activated by DNA double-strand breaks (DSBs) and single-stranded DNA respectively. |
|
| 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 |
| + |
DNA_damage | up-regulates
|
SLX4 |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259063 |
|
|
in vitro |
|
| pmid |
sentence |
| 10542278 |
HMLH1 and hPMS2 function in postreplicative mismatch repair in the form of a heterodimer referred to as hMutLα. Tumors or cell lines lacking this factor display mutator phenotypes and microsatellite instability, and mutations in the hMLH1 andhPMS2 genes predispose to hereditary non-polyposis colon cancer. Recombinant hMutLα and hMutLβ, expressed in the baculovirus system, were tested for their activity in an in vitro mismatch repair assay. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| Pathways: | DNA repair in cancer |
| + |
DNA_damage | up-regulates
|
TAOK1 |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-226599 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17396146 |
These findings indicate that TAO kinases are regulators of p38-mediated responses to DNA damage and are intermediates in the activation of p38 by ATM. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | P38 Signaling |
| + |
DNA_damage | up-regulates
|
XAB2 |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-275692 |
|
|
|
|
| pmid |
sentence |
| 24086043 |
TC-NER is initiated by RNA polymerase stalled at a lesion with the help of TC-NER specific factors CSA, CSB, and XAB2. |
|
| Publications: |
1 |
| + |
DNA_damage | up-regulates activity
|
PALB2 |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-244490 |
|
|
Homo sapiens |
U2-OS Cell |
| pmid |
sentence |
| 19369211 |
Consistent with the converging functions of the BRCA proteins in DNA repair, cells harboring mutations with abrogated BRCA1-PALB2 interaction resulted in defective homologous recombination (HR) repair. We propose that, via its direct interaction with PALB2, BRCA1 fine-tunes recombinational repair partly through its modulatory role in the PALB2-dependent loading of BRCA2-RAD51 repair machinery at DNA breaks. Our findings uncover PALB2 as the molecular adaptor between the BRCA proteins, and suggest that impaired HR repair is one of the fundamental causes for genomic instability and tumorigenesis observed in patients carrying BRCA1, BRCA2, or PALB2 mutations. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | DNA repair in cancer |
| + |
DNA_damage | up-regulates
|
MLH1/PMS2 |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259062 |
|
|
in vitro |
|
| pmid |
sentence |
| 10542278 |
HMLH1 and hPMS2 function in postreplicative mismatch repair in the form of a heterodimer referred to as hMutLα. Tumors or cell lines lacking this factor display mutator phenotypes and microsatellite instability, and mutations in the hMLH1 andhPMS2 genes predispose to hereditary non-polyposis colon cancer. Recombinant hMutLα and hMutLβ, expressed in the baculovirus system, were tested for their activity in an in vitro mismatch repair assay. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| Pathways: | DNA repair in cancer |
| + |
DNA_damage | up-regulates
|
TAOK2 |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-226602 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17396146 |
These findings indicate that TAO kinases are regulators of p38-mediated responses to DNA damage and are intermediates in the activation of p38 by ATM. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | P38 Signaling |
| + |
DNA_damage | up-regulates activity
|
ATM |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253376 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 12556884 |
Cellular irradiation induces rapid intermolecular autophosphorylation of serine 1981 that causes dimer dissociation and initiates cellular ATM kinase activity. Most ATM molecules in the cell are rapidly phosphorylated on this site after doses of radiation as low as 0.5 Gy, and binding of a phosphospecific antibody is detectable after the introduction of only a few DNA double-strand breaks in the cell. Activation of the ATM kinase seems to be an initiating event in cellular responses to irradiation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Colorectal Carcinoma, DNA repair in cancer, FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, p53 in cancer |
| + |
DNA_damage | up-regulates
|
Fanconi anemia core complex |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263251 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 17396147 |
The Fanconi anemia (FA) core complex plays a central role in the DNA damage response network involving breast cancer susceptibility gene products, BRCA1 and BRCA2. The complex consists of eight FA proteins, including a ubiquitin ligase (FANCL) and a DNA translocase (FANCM), and is essential for monoubiquitination of FANCD2 in response to DNA damage. |
|
| 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 |
| + |
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 |
| + |
DNA_damage | up-regulates activity
|
CDKN2A |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-245493 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25101116 |
ARF: a versatile DNA damage response ally at the crossroads of development and tumorigenesis. Alternative reading frame (ARF) is a tumor suppressor protein that senses oncogenic and other stressogenic signals. It can trigger p53-dependent and -independent responses with cell cycle arrest and apoptosis induction being the most prominent ones. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition |
| + |
DNA_damage | up-regulates
|
RAD23B |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-275688 |
|
|
|
|
| pmid |
sentence |
| 24086043 |
GG-NER is initiated by the GG-NER specific factor XPC-RAD23B, in some cases with the help of UV-DDB (UV-damaged DNA-binding protein). |
|
| Publications: |
1 |
| + |
DNA_damage | up-regulates
|
RAD23A |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-275686 |
|
|
|
|
| pmid |
sentence |
| 24086043 |
GG-NER is initiated by the GG-NER specific factor XPC-RAD23B, in some cases with the help of UV-DDB (UV-damaged DNA-binding protein). |
|
| Publications: |
1 |
| + |
DNA_damage | up-regulates
|
PARP1 |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260065 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17891139 |
We identify the major poly(ADP-ribosyl)ated sites of p53 by PARP-1 and find that PARP-1-mediated poly(ADP-ribosyl)ation blocks the interaction between p53 and the nuclear export receptor Crm1, resulting in nuclear accumulation of p53. These findings molecularly link PARP-1 and p53 in the DNA-damage response, providing the mechanism for how p53 accumulates in the nucleus in response to DNA damage.|PARP-1 is super-activated by binding to damaged DNA, and poly(ADP-ribosyl)ates p53. Poly(ADP-ribosyl)ation probably induces a structural change that mask the NES, and thus Crm1 can no longer target p53 to the nuclear export machinery, resulting in accumulation of p53 in the nucleus. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | FLT3-ITD signaling, Mitochondrial Control of Apoptosis |
| + |
DNA_damage | up-regulates
|
KDM4B |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263736 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 30759871 |
The KDM4 family of Jumonj domain histone demethylases specifically target di- and tri-methylated lysine 9 on histone H3 (H3K9me3), removing a modification central to defining heterochromatin and gene repression. KDM4 enzymes are generally over-expressed in cancers, making them compelling targets for study and therapeutic inhibition. One of these family members, KDM4B, is especially interesting due to its regulation by multiple cellular stimuli, including DNA damage, steroid hormones, and hypoxia. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
3.0
DNA_damage