Render Target: SSR
Render Timestamp: 2024-12-19T21:30:36.838Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-04-05 20:32:29.086
Product last modified at: 2024-12-17T18:55:11.429Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77

Phospho-ATM (Ser1981) (10H11.E12) Mouse mAb #4526

Filter:
  • WB

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 350
    Source/Isotype Mouse IgG1
    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) (10H11.E12) Mouse mAb detects endogenous levels of ATM only when phosphorylated at Ser1981.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic phosphopeptide corresponding to residues around Ser1981 of human ATM.

    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).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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    This product is sold under license, U.S. Patent Publication numbers 2003/0077661 and 2003/0157572, from St. Jude Childrens Research Hospital.
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