Ataxia telangiectasia mutated kinase (ATM) and ataxia telangiectasia and Rad3-related kinase (ATR) are related kinases that regulate cell cycle checkpoints and DNA repair. Mutation in the ATM gene results in the autosomal recessive disease ataxia telangiectasia (AT). The identified substrates for ATM are p53, p95/NBS1, MDM2, Chk2, BRCA1, CtIP, 4E-BP1 and Chk1. The essential requirement for the substrates of ATM/ATR is S/TQ. Hydrophobic amino acids at positions -3 and -1, and negatively charged amino acids at position +1 are positive determinants for substrate recognition by these kinases. Positively charged residues surrounding the S/TQ are negative determinants for substrate phosphorylation. The complex phenotype of cells derived from patients with AT suggests that ATM has additional cellular substrates. In unirradiated cells, ATM is present as an inactive homodimer or multimer. Double-stranded breaks in DNA caused by ionizing radiation cause rapid ATM kinase activation through dissociation of this complex and ATM autophosphorylation at Ser1981.
Synonyms: A-T, mutated, AT mutated, TEL1, telomere maintenance 1, homolog, ataxia telangiectasia mutated, ataxia telangiectasia mutated (includes complementation groups A, C and D), ataxia telangiectasia mutated protein, human phosphatidylinositol 3-kinase homolog
Application: Use Anti-phospho-ATM (Ser1981) Antibody, clone 10H11.E12 (Mouse Monoclonal Antibody) validated in ICC, IF, IP, WB to detect phospho-ATM (Ser1981) also known as A-T mutated.
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Other Notes: Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.