Relation Results

Summary

Name DNA_damage
Primary ID SIGNOR-ST1
Type stimulus
Description DNA Damage
Relations 21
Pathways Colorectal Carcinoma, DNA repair in cancer, FLT3-ITD signaling, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, GPCR_CRC, Mitochondrial Control of Apoptosis, Myogenesis modulation: DNA damage, Non-small-cell lung cancer (NSCLC), P38 Signaling, p53 in cancer, Satellite: DDR inhibition

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Type: Score: Layout: SPV 
0.70.70.70.70.70.70.70.70.70.70.70.70.70.70.70.70.70.70.70.7DNA_damageSLX4TAOK1ERCC6TTKFanconi anemia core complexPARP1TAOK2KDM4BTP53RAD23AATMRAD23BCHEK2ERCC8CHEK1ATRPALB2MLH1/PMS2XAB2CDKN2A

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Relations
Regulator
Mechanism
target
score ℹ
+ DNA_damageup-regulates img/indirect-activation.png SLX4 0.7
Identifier Residue Sequence Organism Cell Line
SIGNOR-259063 in vitro
pmid sentence
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_damageup-regulates img/indirect-activation.png TAOK1 0.7
Identifier Residue Sequence Organism Cell Line
SIGNOR-226599 Homo sapiens
pmid sentence
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_damageup-regulates img/indirect-activation.png ERCC6 0.7
Identifier Residue Sequence Organism Cell Line
SIGNOR-275691
pmid sentence
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_damageup-regulates img/indirect-activation.png TTK 0.7
Identifier Residue Sequence Organism Cell Line
SIGNOR-242619 Homo sapiens
pmid sentence
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_damageup-regulates img/indirect-activation.png Fanconi anemia core complex 0.7
Identifier Residue Sequence Organism Cell Line
SIGNOR-263251 Homo sapiens HeLa Cell
pmid sentence
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_damageup-regulates img/indirect-activation.png PARP1 0.7
Identifier Residue Sequence Organism Cell Line
SIGNOR-260065 Homo sapiens
pmid sentence
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_damageup-regulates img/indirect-activation.png TAOK2 0.7
Identifier Residue Sequence Organism Cell Line
SIGNOR-226602 Homo sapiens
pmid sentence
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_damageup-regulates img/indirect-activation.png KDM4B 0.7
Identifier Residue Sequence Organism Cell Line
SIGNOR-263736 Homo sapiens
pmid sentence
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
+ DNA_damageup-regulates quantity img/indirect-activation.png TP53 0.7
Identifier Residue Sequence Organism Cell Line
SIGNOR-209690 Homo sapiens
pmid sentence
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_damageup-regulates img/indirect-activation.png RAD23A 0.7
Identifier Residue Sequence Organism Cell Line
SIGNOR-275686
pmid sentence
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_damageup-regulates img/indirect-activation.png ATM 0.7
Identifier Residue Sequence Organism Cell Line
SIGNOR-242612 Homo sapiens
pmid sentence
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_damageup-regulates img/indirect-activation.png RAD23B 0.7
Identifier Residue Sequence Organism Cell Line
SIGNOR-275688
pmid sentence
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_damageup-regulates activity img/indirect-activation.png CHEK2 0.7
Identifier Residue Sequence Organism Cell Line
SIGNOR-242605 Homo sapiens
pmid sentence
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_damageup-regulates img/indirect-activation.png ERCC8 0.7
Identifier Residue Sequence Organism Cell Line
SIGNOR-275690
pmid sentence
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_damageup-regulates img/indirect-activation.png CHEK1 0.7
Identifier Residue Sequence Organism Cell Line
SIGNOR-242616 Homo sapiens
pmid sentence
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_damageup-regulates img/indirect-activation.png ATR 0.7
Identifier Residue Sequence Organism Cell Line
SIGNOR-242609 Homo sapiens
pmid sentence
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_damageup-regulates activity img/indirect-activation.png PALB2 0.7
Identifier Residue Sequence Organism Cell Line
SIGNOR-244490 Homo sapiens U2-OS Cell
pmid sentence
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_damageup-regulates img/indirect-activation.png MLH1/PMS2 0.7
Identifier Residue Sequence Organism Cell Line
SIGNOR-259062 in vitro
pmid sentence
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_damageup-regulates img/indirect-activation.png XAB2 0.7
Identifier Residue Sequence Organism Cell Line
SIGNOR-275692
pmid sentence
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_damageup-regulates activity img/indirect-activation.png ATM 0.7
Identifier Residue Sequence Organism Cell Line
SIGNOR-253376 Homo sapiens HEK-293 Cell
pmid sentence
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_damageup-regulates activity img/indirect-activation.png CDKN2A 0.7
Identifier Residue Sequence Organism Cell Line
SIGNOR-245493 Homo sapiens
pmid sentence
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
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