Product Pathways - DNA Damage
MSH2 (D24B5) XP® Rabbit mAb #2017
|W IP IHC-P IF-IC F||H M||Endogenous||100||Rabbit IgG|
Reactivity Key: H=Human M=Mouse
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.
Specificity / Sensitivity
MSH2 (D24B5) XP® Rabbit mAb detects endogenous levels of total MSH2 protein.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues at the amino terminus of human MSH2.
Western blot analysis of extracts of HeLa and NIH/3T3 cells using MSH2 (D24B5) XP® Rabbit mAb.
Immunohistochemical analysis of paraffin-embedded human breast carcinoma using MSH2 (D24B5) XP® Rabbit mAb in the presence of control peptide (left) or antigen-specific peptide (right).
Flow cytometric analysis of HeLa cells using MSH2 (D24B5) XP® Rabbit mAb (blue) compared to a nonspecific negative control antibody (red).
The DNA mismatch repair system (MMR) repairs post-replication DNA, inhibits recombination between non-identical DNA sequences and induces both checkpoint and apoptotic responses following certain types of DNA damage (1). MSH2 (MutS homologue 2) forms the hMutS-α dimer with MSH6 and is an essential component of the mismatch repair process. hMutS-α is part of the BRCA1-associated surveillance complex (BASC), a complex that also contains BRCA1, MLH1, ATM, BLM, PMS2 proteins and the Rad50-Mre11-NBS1 complex (2).Mutations in MSH2 have been found in a large proportion of hereditary non-polyposis colorectal cancer (Lynch Syndrome), the most common form of inherited colorectal cancer in the Western world (3). Mutations have also been associated with other sporadic tumors.
- O'Brien, V. and Brown, R. (2006) Carcinogenesis 27, 682-92.
- Wang, Y. et al. (2000) Genes Dev 14, 927-39.
- Plotz, G. et al. (2006) J Mol Histol 37, 271-83.
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For Research Use Only. Not For Use In Diagnostic Procedures.