Render Target: SSR
Render Timestamp: 2024-12-26T19:20:37.963Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-09-20 06:17:04.817
Product last modified at: 2024-12-17T13:00:14.536Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

Mre11 Antibody #4895

Filter:
  • WB
  • IP
  • IHC

    Supporting Data

    REACTIVITY H M R Mk
    SENSITIVITY Endogenous
    MW (kDa) 81
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • IHC-Immunohistochemistry 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 
    • Mk-Monkey 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:100
    Immunohistochemistry (Paraffin) 1:500

    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

    Mre11 Antibody detects endogenous levels of Mre11 homologue A (Mre11A). The antibody may cross-react with Mre11 homologue B (Mre11B).

    Species Reactivity:

    Human, Mouse, Rat, Monkey

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Lys496 of human Mre11A. Antibodies are purified by protein A and peptide affinity chromatography.

    Background

    Mre11, originally described in genetic screens from the yeast Saccharomyces cerevisiae in which mutants were defective in meiotic recombination (1), is a central part of a multisubunit nuclease composed of Mre11, Rad50 and Nbs1 (MRN) (2,3). The MRN complex plays a critical role in sensing, processing and repairing DNA double strand breaks. Defects lead to genomic instability, telomere shortening, aberrant meiosis and hypersensitivity to DNA damage (4). Hypomorphic mutations of Mre11 are found in ataxia-telangiectasia-like disease (ATLD), with phenotypes similar to mutations in ATM that cause ataxia-telangiectasia (A-T), including a predisposition to malignancy in humans (5). Cellular consequences of ATLD include chromosomal instability and defects in the intra-S phase and G2/M checkpoints in response to DNA damage. The MRN complex may directly activate the ATM checkpoint kinase at DNA breaks (6).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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