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
ATM
Gene Ontology Biological Process
- DNA damage induced protein phosphorylation [IDA]
- DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrest [TAS]
- DNA repair [TAS]
- cell cycle arrest [IMP]
- cellular response to DNA damage stimulus [IMP]
- cellular response to gamma radiation [IDA]
- double-strand break repair [TAS]
- double-strand break repair via homologous recombination [TAS]
- histone mRNA catabolic process [IDA]
- mitotic spindle assembly checkpoint [IMP]
- negative regulation of B cell proliferation [IMP]
- peptidyl-serine phosphorylation [IDA]
- phosphatidylinositol-3-phosphate biosynthetic process [IMP]
- positive regulation of DNA damage response, signal transduction by p53 class mediator [IMP]
- positive regulation of apoptotic process [IMP]
- pre-B cell allelic exclusion [ISS]
- protein autophosphorylation [IDA]
- protein phosphorylation [IDA]
- reciprocal meiotic recombination [TAS]
- replicative senescence [IMP]
- response to ionizing radiation [IDA]
- signal transduction [TAS]
- signal transduction involved in mitotic G2 DNA damage checkpoint [IMP]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Protein-peptide
An interaction is detected between a protein and a peptide derived from an interaction partner. This includes phage display experiments.
Publication
Substrate specificities and identification of putative substrates of ATM kinase family members.
Ataxia telangiectasia mutated (ATM) phosphorylates p53 protein in response to ionizing radiation, but the complex phenotype of AT cells suggests that it must have other cellular substrates as well. To identify substrates for ATM and the related kinases ATR and DNA-PK, we optimized in vitro kinase assays and developed a rapid peptide screening method to determine general phosphorylation consensus sequences. ... [more]
Throughput
- Low Throughput
Additional Notes
- in vitro kinase assay using GST-peptide substrates
Related interactions
| Interaction | Experimental Evidence Code | Dataset | Throughput | Score | Curated By | Notes |
|---|---|---|---|---|---|---|
| ATR ATM | 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 | 467651 | |
| ATM ATR | 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 | - |
Curated By
- BioGRID