Chromosomes are constantly damaged by exogenous and endogenous factors. To cope with DNA damage, eukaryotic cells are equipped with three phosphatidylinositol 3-kinase-related kinases (PIKKs), such as ATM, ATR, and DNA-PK. PIKKs are structurally related to phosphatidylinositol 3-kinase (lipid kinase), however possess protein kinase activities. The Mre11-Rad50-Nbs1 and the Ku complex interact with and activate ATM and DNA-PKcs at double-stranded DNA breaks (DSBs), respectively. In contrast, ATR responds to various types of DNA lesions by interacting with replication protein A (RPA)-covered single-stranded DNA (ssDNA). Several lines of evidence have established a model in which ATR is activated by interacting with ATR activating proteins including TopBP1 and ETAA1 at DNA lesions in humans, yet the interaction of ATR with RPA-covered ssDNA does not result in ATR activation. In budding yeast, the Mec1-Ddc2 complex (Mec1-Ddc2) corresponds to ATR-ATRIP. Similar to ATR, Mec1 activation is accomplished by interactions with Mec1 activating proteins, which are Ddc1, Dpb11 (TopBP1 homolog) and Dna2. However, recent studies provide results supporting the idea that Mec1ATR is also activated by interacting with RPA-covered ssDNA tracts. These observations suggest that all the ATM, ATR, DNA-PK family proteins can be activated immediately upon DNA damage recognition.
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| Evidence ID | Analyze ID | Gene/Complex | Systematic Name/Complex Accession | Qualifier | Gene Ontology Term ID | Gene Ontology Term | Aspect | Annotation Extension | Evidence | Method | Source | Assigned On | Reference |
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| Evidence ID | Analyze ID | Gene | Gene Systematic Name | Phenotype | Experiment Type | Experiment Type Category | Mutant Information | Strain Background | Chemical | Details | Reference |
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| Evidence ID | Analyze ID | Gene | Gene Systematic Name | Disease Ontology Term | Disease Ontology Term ID | Qualifier | Evidence | Method | Source | Assigned On | Reference |
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| Evidence ID | Analyze ID | Regulator | Regulator Systematic Name | Target | Target Systematic Name | Direction | Regulation of | Happens During | Regulator Type | Direction | Regulation Of | Happens During | Method | Evidence | Strain Background | Reference |
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| Site | Modification | Modifier | Source | Reference |
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| Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Allele | Assay | Annotation | Action | Phenotype | SGA score | P-value | Source | Reference | Note |
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| Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Assay | Annotation | Action | Modification | Source | Reference | Note |
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| Complement ID | Locus ID | Gene | Species | Gene ID | Strain background | Direction | Details | Source | Reference |
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| Evidence ID | Analyze ID | Dataset | Description | Keywords | Number of Conditions | Reference |
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