ATM (Ser-1981), phospho-specific (clone M366), anti-human, mouse, rat

Background:
Ataxia telangiectasia mutated kinase (ATM) is a serine/threonine kinase that regulates cell cycle checkpoints and DNA repair. Mutations of ATM cause a spectrum of defects ranging from neurodegeneration to cancer predisposition. Activation of ATM after DNA damage involves Cdk5 mediated phosphorylation of Ser-794 followed by autophosphorylation at Ser-1891. Active ATM kinase regulates a number of proteins involved in cell cycle checkpoint control, apoptosis and DNA repair. The Cdk5–ATM pathway regulates phosphorylation and function of the ATM targets p53 and H2AX in postmitotic neurons. Other known substrates of ATM include Chk2, Chk1, CtIP, 4E-BP1, BRCA1, RPA3, SMC1, FANCD2, Rad17, Artemis, Nbs1, and the I-2 regulatory subunit of PP1. Thus, activation of Cdk5 by DNA damage may be an important initiator of ATM-dependent regulation of cell cycle checkpoints.

Immunogen: Clone M366 was generated from a phospho-peptide that included amino acids surrounding Serine 1981 in human ATM. This sequence has high homology to the conserved site in rat and mouse ATM.

Specificity: This antibody detects a 370 kDa* protein corresponding to the molecular mass of ATM on SDS-PAGE immunoblots of calyculin A treated human A431 and Jurkat Cells, but is not observed in control cells.

Application dilution:
ELISA: 1:2000
ICC: 1:200
IP: 1:100
WB: 1:1000
End user should determine optimal dilution for their particular applications and experiments.Western blot membranes were incubated with diluted antibody in 5% non-fat milk, PBS, 0.04% Tween20 for 1 hour at room temperature.

Buffer/Storage:
Mouse monoclonal, protein A purified antibody is supplied in 100µl phosphate-buffered saline, 50% glycerol, 1 mg/ml BSA, and 0.05% sodium azide. Store at -20°C. Stable for 1 year.