Render Target: STATIC
Render Timestamp: 2024-10-03T10:27:51.311Z
Commit: f04ddd7fea9fb3592f59f61482fcb94610d25cbe
1% for the planet logo
PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77

Mre11 (31H4) Rabbit mAb #4847

Filter:
  • WB
  • IP
  • IHC

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 81
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • IHC-Immunohistochemistry 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:50
    Immunohistochemistry (Paraffin) 1:500 - 1:2000

    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

    Mre11 detects endogenous levels of Mre11 homologue A (Mre11A).

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Lys496 of human Mre11A.

    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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