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
FANCI
Gene Ontology Biological Process
Gene Ontology Molecular Function
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
ATR-ATRIP kinase complex triggers activation of the Fanconi anemia DNA repair pathway.
ATR kinase activates the S-phase checkpoint when replication forks stall at sites of DNA damage. This event also causes phosphorylation of the Fanconi anemia (FA) protein FANCI, triggering its monoubiquitination of the key DNA repair factor FANCD2 by the FA core E3 ligase complex, thereby promoting this central pathway of DNA repair which permits replication to be restarted. However, the ... [more]
Throughput
- Low Throughput
Curated By
- BioGRID