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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

Mre11 Antibody #4895

Filter:
  • WB
  • IP
  • IHC
Western Blotting Image 1: Mre11 Antibody
Western blot analysis of extracts from Jurkat (human), L929 (mouse), Neuro-2a (mouse) and C6 (rat) cells, using Mre11 Antibody.

To Purchase # 4895

Cat. # Size Qty. Price Ships
4895S 100 µl
$306 Jan 22

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 
  • Related Products

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).

Pathways

Explore pathways related to this product.


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