CHK1
Gene Ontology Biological Process
- mitotic DNA damage checkpoint [IGI]
- mitotic G2 DNA damage checkpoint [IMP]
- negative regulation of transcription from RNA polymerase II promoter by transcription factor localization involved in response to DNA damage checkpoint signaling [IMP]
- peptidyl-serine phosphorylation [IDA]
- signal transduction involved in DNA damage checkpoint [IMP]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
WEE1
Gene Ontology Biological Process
- cytokinesis after mitosis checkpoint [IGI]
- mitotic DNA damage checkpoint [IMP]
- mitotic cell cycle checkpoint [IMP]
- negative regulation of G2/M transition of mitotic cell cycle [IMP]
- negative regulation of protein kinase activity by regulation of protein phosphorylation [IDA]
- peptidyl-serine autophosphorylation [IDA]
- peptidyl-tyrosine autophosphorylation [IDA]
- regulation of cell size [NAS]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Biochemical Activity (Phosphorylation)
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.
Publication
Chk1 is a wee1 kinase in the G2 DNA damage checkpoint inhibiting cdc2 by Y15 phosphorylation.
The G2 DNA damage checkpoint ensures maintenance of cell viability by delaying progression into mitosis in cells which have suffered genomic damage. It is controlled by a number of proteins which are hypothesized to transduce signals through cell cycle regulators to delay activation of p34cdc2. Studies in mammalian cells have correlated induction of inhibitory tyrosine 15 (Y15) phosphorylation on p34cdc2 ... [more]
Throughput
- Low Throughput
Related interactions
| Interaction | Experimental Evidence Code | Dataset | Throughput | Score | Curated By | Notes |
|---|---|---|---|---|---|---|
| WEE1 CHK1 | Phenotypic Enhancement Phenotypic Enhancement A genetic interaction is inferred when mutation or overexpression of one gene results in enhancement of any phenotype (other than lethality/growth defect) associated with mutation or over expression of another gene. | Low | - | BioGRID | 737546 | |
| WEE1 CHK1 | Synthetic Lethality 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. | Low | - | BioGRID | 2334305 | |
| CHK1 WEE1 | Synthetic Lethality 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. | Low | - | BioGRID | 246804 | |
| CHK1 WEE1 | Synthetic Lethality 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. | Low | - | BioGRID | 247236 | |
| CHK1 WEE1 | Synthetic Rescue Synthetic Rescue A genetic interaction is inferred when mutations or deletions of one gene rescues the lethality or growth defect of a strain mutated or deleted for another gene. | Low | - | BioGRID | 666528 |
Curated By
- BioGRID