CHEK2
Gene Ontology Biological Process
- DNA damage checkpoint [TAS]
- DNA damage induced protein phosphorylation [IMP]
- G2/M transition of mitotic cell cycle [IMP]
- cellular protein catabolic process [IMP]
- cellular response to DNA damage stimulus [IMP, TAS]
- double-strand break repair [IMP]
- intrinsic apoptotic signaling pathway in response to DNA damage [IDA, IMP]
- positive regulation of transcription, DNA-templated [IDA]
- protein autophosphorylation [IDA]
- protein phosphorylation [IDA]
- protein stabilization [IDA]
- regulation of protein catabolic process [IMP]
- regulation of transcription, DNA-templated [IDA]
- replicative senescence [NAS]
- signal transduction in response to DNA damage [IDA]
- signal transduction involved in intra-S DNA damage checkpoint [IMP]
- spindle assembly involved in mitosis [IMP]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
ATR
Gene Ontology Biological Process
- DNA damage checkpoint [IDA]
- DNA repair [TAS]
- DNA replication [TAS]
- cell cycle [TAS]
- cellular response to DNA damage stimulus [TAS]
- cellular response to UV [IMP]
- cellular response to gamma radiation [IDA]
- double-strand break repair via homologous recombination [IBA]
- multicellular organismal development [TAS]
- negative regulation of DNA replication [IMP]
- peptidyl-serine phosphorylation [IDA]
- positive regulation of DNA damage response, signal transduction by p53 class mediator [IMP]
- protein autophosphorylation [IDA]
- replicative senescence [IMP]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Synthetic Lethality
A genetic interaction is inferred when mutations or deletions in separate genes, each of which alone causes a minimal phenotype, result in lethality when combined in the same cell under a given condition.
Publication
A Network of Conserved Synthetic Lethal Interactions for Exploration of Precision Cancer Therapy.
An emerging therapeutic strategy for cancer is to induce selective lethality in a tumor by exploiting interactions between its driving mutations and specific drug targets. Here we use a multi-species approach to develop a resource of synthetic lethal interactions relevant to cancer therapy. First, we screen in yeast ∼169,000 potential interactions among orthologs of human tumor suppressor genes (TSG) and ... [more]
Throughput
- High Throughput
Ontology Terms
- phenotype: growth abnormality (HP:0001507) [hela cell (BTO:0000567)]
Additional Notes
- CHEK1,CHEK2 double mutant as drug target
- Chemo-genetic screen with siRNAs
- Drug AZD7762
- HeLa cervical cancer cell line
Related interactions
| Interaction | Experimental Evidence Code | Dataset | Throughput | Score | Curated By | Notes |
|---|---|---|---|---|---|---|
| ATR CHEK2 | Biochemical Activity Biochemical Activity An interaction is inferred from the biochemical effect of one protein upon another, for example, GTP-GDP exchange activity or phosphorylation of a substrate by a kinase. The bait protein executes the activity on the substrate hit protein. A Modification value is recorded for interactions of this type with the possible values Phosphorylation, Ubiquitination, Sumoylation, Dephosphorylation, Methylation, Prenylation, Acetylation, Deubiquitination, Proteolytic Processing, Glucosylation, Nedd(Rub1)ylation, Deacetylation, No Modification, Demethylation. | Low | - | BioGRID | 589886 | |
| ATR CHEK2 | Biochemical Activity Biochemical Activity An interaction is inferred from the biochemical effect of one protein upon another, for example, GTP-GDP exchange activity or phosphorylation of a substrate by a kinase. The bait protein executes the activity on the substrate hit protein. A Modification value is recorded for interactions of this type with the possible values Phosphorylation, Ubiquitination, Sumoylation, Dephosphorylation, Methylation, Prenylation, Acetylation, Deubiquitination, Proteolytic Processing, Glucosylation, Nedd(Rub1)ylation, Deacetylation, No Modification, Demethylation. | Low | - | BioGRID | 470464 |
Curated By
- BioGRID