ATM (Ser-794), phospho-specific polyclonal, 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: Phospho-ATM (Ser-794) synthetic peptide (coupled to carrier protein) corresponding to amino acids surrounding Ser-794 in human ATM. This sequence is well conserved in rat and mouse ATM.

Specificity: This antibody was affinity purified using phospho-ATM (Ser-794) peptide (without carrier). The antibody detects a 370 kDa* band corresponding to ATM on SDS-PAGE immunoblots of calyculin A treated Jurkat, A431, HeLa, and rat PC12 cells. This reactivity is removed after lambda phosphatase treatment.

Buffer/Storage:
Rabbit polyclonal, affinity-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.