Cell Signaling Technology

Product Pathways - DNA Damage

Mre11 (31H4) Rabbit mAb #4847

Applications Reactivity MW (kDa) Source Isotype
W IP IHC-P IHC-F IF-IC F H 81 Rabbit IgG

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

Specificity / Sensitivity

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

Source / Purification

Rabbit monoclonal antibodies are produced by immunizing rabbits with a synthetic peptide (KLH-coupled) corresponding to residues surrounding Lys496 of human Mre11A.

Western Blotting

Western Blotting

Western blot analysis of extracts from HeLa and K562 cells, using Mre11 Rabbit (31H4) mAb.

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human breast carcinoma, using Mre11 (31H4) Rabbit mAb in the presence of control peptide (left) or Mre11 Blocking Peptide #1035 (right).

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded lung carcinoma, using Mre11 (31H4) Rabbit mAb.


IHC-F (frozen)

IHC-F (frozen)

Immunohistochemical analysis of frozen SKOV-3 xenograft using Mre11 (31H4) Rabbit mAb.

Flow Cytometry

Flow Cytometry

Flow cytometric analysis of K562 cells, using Mre11 (31H4) Rb mAb (blue) compared to a nonspecific negative control antibody (red).

IF-IC

IF-IC

Immunofluorescence staining of HeLa cells showing nuclear staining, using Mre11 (31H4) Rabbit mAb.


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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Companion Products

Rabbit Monoclonals Produced Using Epitomics® Technology, U.S. Patent No. 5,675,063.

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