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
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
Depletion of ATR selectively sensitizes ATM-deficient human mammary epithelial cells to ionizing radiation and DNA-damaging agents.
DNA damage response (DDR) to double strand breaks is coordinated by 3 phosphatidylinositol 3-kinase-related kinase (PIKK) family members: the ataxia-telangiectasia mutated kinase (ATM), the ATM and Rad3-related (ATR) kinase and the catalytic subunit of the DNA-dependent protein kinase (DNA-PKcs). ATM and ATR are central players in activating cell cycle checkpoints and function as an active barrier against genome instability and ... [more]
Throughput
- Low Throughput
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 | |
| ATR ATM | Protein-peptide Protein-peptide An interaction is detected between a protein and a peptide derived from an interaction partner. This includes phage display experiments. | Low | - | BioGRID | 245114 |
Curated By
- BioGRID