Cell Signaling Technology

Product Pathways - DNA Damage

Mre11 Antibody #4895

Applications Reactivity MW (kDa) Source
W IP IHC-P IHC-F IF-IC H M R Mk 81 Rabbit

Applications Key:  W=Western Blotting  IP=Immunoprecipitation  IHC-P=Immunohistochemistry (Paraffin)  IHC-F=Immunohistochemistry (Frozen)  IF-IC=Immunofluorescence (Immunocytochemistry)
Reactivity Key:  H=Human  M=Mouse  R=Rat  Mk=Monkey
Species enclosed in parentheses are predicted to react based on 100% sequence homology. Species cross-reactivity is determined by Western blot.

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 rabbits with a synthetic peptide (KLH-coupled) corresponding to residues surrounding Lys496 of human Mre11A. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from Jurkat (human), L929 (mouse), Neuro-2a (mouse) and C6 (rat) cells, using Mre11 Antibody.

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human colon carcinoma, showing nuclear localization, using Mre11 Antibody.

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human breast carcinoma, using Mre11 Antibody in the presence of control peptide (left) or Mre11 Blocking Peptide #1035 (right).


IHC-F (frozen)

IHC-F (frozen)

Immunohistochemical analysis of H1650 xenograft, using Mre11 Antibody.

IF-IC

IF-IC

Immunofluorescent analysis of HeLa cells, showing nuclear localization, using Mre11 Antibody.

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).

  1. Ajimura, M. et al. (1993) Genetics 133, 51-66.
  2. D'Amours, D. and Jackson, S.P. (2002) Nat. Rev. Mol. Cell Biol. 3, 317-327.
  3. van den Bosch, M. et al. (2003) EMBO Rep. 4, 844-849.
  4. Theuissen, J.F. et al. (2003) Mol. Cell 12, 1511-1523.
  5. Stewart, G.S. et al. (1999) Cell 99, 577-587.
  6. Carson, C.T. et al. (2003) EMBO J. 22, 6610-6620.

Application References

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