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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