Render Target: STATIC
Render Timestamp: 2024-11-18T12:01:27.015Z
Commit: 3c1f305a63297e594ac8d7bb5424007d592d68be
XML generation date: 2024-08-01 15:26:57.189
Product last modified at: 2024-11-15T14:15:08.424Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

53BP1 Antibody #4937

Filter:
  • WB
  • IHC
  • IF

    Supporting Data

    REACTIVITY H Mk
    SENSITIVITY Endogenous
    MW (kDa) 450
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    • IHC-Immunohistochemistry 
    • IF-Immunofluorescence 
    Species Cross-Reactivity Key:
    • H-Human 
    • Mk-Monkey 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunohistochemistry (Paraffin) 1:100
    Immunofluorescence (Immunocytochemistry) 1:100

    Storage

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

    Protocol

    Specificity / Sensitivity

    53BP1 Antibody detects endogenous levels of total 53BP1 protein independent of phosphorylation.

    Species Reactivity:

    Human, Monkey

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues near the center of human 53BP1. Antibodies are purified by protein A and peptide affinity chromatography.

    Background

    p53-binding protein 1 (53BP1) was originally identified as a p53 binding partner that could enhance the transcriptional activity of p53 (1,2). 53BP1 consists of two BRCA1 carboxy terminal (BRCT) domains that allow for binding to p53 and a separate domain responsible for binding to phosphorylated histone H2A.X (3). 53BP1 rapidly translocates to nuclear foci following treatment of cells with ionizing radiation (IR) or radiomimetic agents that cause DNA double strand breaks (DSBs) (4,5). Because of this localization to DSBs and homology to the yeast protein Rad9, a role for 53BP1 in DSB repair has been proposed. Recruitment of 53BP1 to sites of DNA damage has been demonstrated to be independent of ATM, NBS1, and DNA-PK (4) and retention of 53BP1 at DNA breaks requires phosphorylated H2A.X (6). In cells lacking 53BP1, phosphorylation of ATM substrates is reduced, suggesting that 53BP1 is upstream of ATM (7). In response to IR, phosphorylation of 53BP1 at serines 6, 25, 29, and 784 by ATM has been demonstrated, but phosphorylation at these sites is not required for localization of 53BP1 to sites of DSBs (6). Phosphorylation of 53BP1 at Ser1618 has been reported to be enriched in human cells arrested in mitosis (8).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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