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ATM (Ser-794), Phosphospecific Antibody

Product Specifications

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.

Synonyms

Ataxia telangiectasia mutated, AT1 ATDC TEL1 TELO1

Swiss Prot

Q13315

Modification Site

Ser-794

Host

Rabbit

Cross Reactivity

Human, Mouse, Rat

Target

ATM (Ser-794)

Clonality

Polyclonal

Isotype

IgG

Conjugation

Unconjugated

Source

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.

Applications

WB, FCM

Purification

Antigen Affinity purification

Dilution

WB (1:300-5000), FCM (1:20-100)

Buffer

PBS + 1 mg/ml BSA, 0.05% NaN3 and 50% glycerol

Modification

Phosphorylation

Storage Conditions

Storage at -20°C is recommended, as aliquots may be taken without freeze/thawing due to presence of 50% glycerol. Stable for at least 1 year at -20°C.

Specificity

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.
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