Anti-phospho-ATM (Ser1981) Antibody, clone 10H11.E12, Alexa Fluor 488

Serine-protein kinase ATM (EC 2.7.11.1; UniProt Q13315; also known as A-T mutated, Ataxia telangiectasia mutated) is encoded by the ATM (also known as AT) gene (Gene ID 472) in human. 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). Known ATM substrates include p53, p95/NBS1, MDM2, Chk2, BRCA1, CtIP, 4E-BP1, and Chk1. The S/TQ sequence constitutes the essential substrates phosphorylation site motif. Hydrophobic amino acids at positions -3 and -1, and negatively charged amino acids at position +1 are positive determinants for substrate phosphorylation, while positively charged residues surrounding the S/TQ are negative determinants. The complex phenotypes of cells derived from patients with AT suggests that ATM has additional cellular substrates. ATM is present as an inactive homodimer or multimer prior to activation. DNA double-stranded breaks induced by ionizing radiation (IR) cause rapid ATM autophosphorylation at Ser1981 in human or the Ser1987 equivalent in mouse.