Phospho-ATM (Ser1981) (D6H9) Rabbit mAb #5883

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Supporting Data

REACTIVITY	H
SENSITIVITY	Endogenous
MW (kDa)	350
Source/Isotype	Rabbit IgG

Application Key:

WB-Western Blotting

Species Cross-Reactivity Key:

H-Human

Product Information

Product Usage Information

Application	Dilution
Western Blotting	1:1000

Storage

Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

Protocol

Specificity / Sensitivity

Phospho-ATM (Ser1981) (D6H9) Rabbit mAb recognizes endogenous levels of ATM protein only when phosphorylated at Ser1981.

Species Reactivity:

Human

The antigen sequence used to produce this antibody shares 100% sequence homology with the species listed here, but reactivity has not been tested or confirmed to work by CST. Use of this product with these species is not covered under our Product Performance Guarantee.

Species predicted to react based on 100% sequence homology:

Monkey, Bovine, Pig, Horse

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Ser1981 of human ATM protein.

Background

ATM (ataxia telangiectasia mutated kinase) is a serine/threonine protein kinase best known for its role in DNA repair signaling in response to DNA double-strand breaks (DSBs). When DSBs occur, the MRE11:RAD50:NBS1 (MRN) sensor complex recruits ATM to sites of DNA damage. ATM then signals to numerous effector proteins, leading to cellular responses including regulation of DNA repair, cell cycle progression, apoptosis, senescence, gene transcription. Along with ATR, DNA-PKcs, SMG1 and mTOR, ATM is a member of the PI3K-like protein kinase (PIKK) family. PIKK family members typically function in response to various types of cellular stress. Substrates of ATM are numerous, and include CHK2, AKT, p53, BRCA1 and DNA-PK (reviewed in 1,3). Inactive ATM exists as a homodimer. In response to DSBs, ATM undergoes autophosphorylation in trans at Ser1981, which leads to dissociation of the complex to become an active monomer (2). Functional DNA repair pathways are important in cellular homeostasis, and defects in these pathways cause genomic instability, which can lead to tumorigenesis (3). Inactivation of ATM results in ataxia telangiectasia (AT), a neurodegenerative disease characterized by predisposition to cancer (4).

Database Links

UniProt ID: Q13315

Entrez-Gene Id: 472

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For Research Use Only. Not For Use In Diagnostic Procedures.

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