Product Pathways - DNA Damage
Mre11 Antibody #4895
|4895S||100 µl (10 western blots)||---||In Stock||---|
|4895||carrier free and custom formulation / quantity||email request|
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|W||1:1000||Human, Mouse, Rat, Monkey||Endogenous||81||Rabbit|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting, IP=Immunoprecipitation, IHC-P=Immunohistochemistry (Paraffin), IHC-F=Immunohistochemistry (Frozen)
Specificity / Sensitivity
Mre11 Antibody detects endogenous levels of Mre11 homologue A (Mre11A). The antibody may cross-react with Mre11 homologue B (Mre11B).
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.
Western blot analysis of extracts from Jurkat (human), L929 (mouse), Neuro-2a (mouse) and C6 (rat) cells, using Mre11 Antibody.
Immunohistochemical analysis of paraffin-embedded human colon carcinoma, showing nuclear localization, using Mre11 Antibody.
Immunohistochemical analysis of paraffin-embedded human breast carcinoma, using Mre11 Antibody in the presence of control peptide (left) or Mre11 Blocking Peptide #1035 (right).
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).
- Ajimura, M. et al. (1993) Genetics 133, 51-66.
- D'Amours, D. and Jackson, S.P. (2002) Nat. Rev. Mol. Cell Biol. 3, 317-327.
- van den Bosch, M. et al. (2003) EMBO Rep. 4, 844-849.
- Theuissen, J.F. et al. (2003) Mol. Cell 12, 1511-1523.
- Stewart, G.S. et al. (1999) Cell 99, 577-587.
- Carson, C.T. et al. (2003) EMBO J. 22, 6610-6620.
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For Research Use Only. Not For Use In Diagnostic Procedures.
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