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Render Timestamp: 2024-11-08T09:41:31.940Z
Commit: 3c1f305a63297e594ac8d7bb5424007d592d68be
XML generation date: 2024-07-15 19:17:06.793
Product last modified at: 2024-10-07T18:15:15.546Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77

Phospho-Histone H2A.X (Ser139) (D7T2V) Mouse mAb (Pacific Blue Conjugate) #93629

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    Supporting Data

    REACTIVITY H M R Mk
    SENSITIVITY Endogenous
    MW (kDa)
    Source/Isotype Mouse IgG1
    Application Key:
    • F-Flow Cytometry 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 
    • Mk-Monkey 

    Product Information

    Product Description

    This Cell Signaling Technology® antibody is conjugated to Pacific Blue™ fluorescent dye under optimal conditions. This antibody is expected to exhibit the same species cross-reactivity as the unconjugated Phospho-Histone H2A.X (Ser139) (D7T2V) Mouse mAb #80312.

    Product Usage Information

    Application Dilution
    Flow Cytometry (Fixed/Permeabilized) 1:50

    Storage

    Supplied in PBS (pH 7.2), less than 0.1% sodium azide, and 2 mg/mL BSA. Store at 4°C. Do not aliquot the antibody. Protect from light. Do not freeze.

    Protocol

    Specificity / Sensitivity

    Phospho-Histone H2A.X (Ser139) (D7T2V) Mouse mAb (Pacific Blue™ Conjugate) recognizes endogenous levels of Histone H2A.X protein only when phosphorylated at Ser139.

    Species Reactivity:

    Human, Mouse, Rat, Monkey

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Ser139 of human Histone H2A.X protein.

    Background

    Histone H2A.X is a variant histone that represents approximately 10% of the total H2A histone proteins in normal human fibroblasts (1). H2A.X is required for checkpoint-mediated cell cycle arrest and DNA repair following double-stranded DNA breaks (1). DNA damage, caused by ionizing radiation, UV-light, or radiomimetic agents, results in rapid phosphorylation of H2A.X at Ser139 by PI3K-like kinases, including ATM, ATR, and DNA-PK (2,3). Within minutes following DNA damage, H2A.X is phosphorylated at Ser139 at sites of DNA damage to generate γ-H2A.X (4). This very early event in the DNA-damage response is required for recruitment of a multitude of DNA-damage response proteins, including MDC1, NBS1, RAD50, MRE11, 53BP1, and BRCA1 (1). In addition to its role in DNA-damage repair, H2A.X is required for DNA fragmentation during apoptosis and is phosphorylated by various kinases in response to apoptotic signals. H2A.X is phosphorylated at Ser139 by DNA-PK in response to cell death receptor activation, c-Jun N-terminal Kinase (JNK1) in response to UV-A irradiation, and p38 MAPK in response to serum starvation (5-8). H2A.X is constitutively phosphorylated on Tyr142 in undamaged cells by WSTF (Williams-Beuren syndrome transcription factor) (9,10). Upon DNA damage, and concurrent with phosphorylation of Ser139, Tyr142 is dephosphorylated at sites of DNA damage by recruited EYA1 and EYA3 phosphatases (9). While phosphorylation at Ser139 facilitates the recruitment of DNA repair proteins and apoptotic proteins to sites of DNA damage, phosphorylation at Tyr142 appears to determine which set of proteins are recruited. Phosphorylation of H2A.X at Tyr142 inhibits the recruitment of DNA repair proteins and promotes binding of pro-apoptotic factors such as JNK1 (9). Mouse embryonic fibroblasts expressing only mutant H2A.X Y142F, which favors recruitment of DNA repair proteins over apoptotic proteins, show a reduced apoptotic response to ionizing radiation (9). Thus, it appears that the balance of H2A.X Tyr142 phosphorylation and dephosphorylation provides a switch mechanism to determine cell fate after DNA damage.
    For Research Use Only. Not For Use In Diagnostic Procedures.
    Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc.
    Pacific Blue is a trademark of Life Technologies Corporation.
    All other trademarks are the property of their respective owners. Visit our Trademark Information page.