Product Pathways - DNA Damage
MSH6 (D60G2) XP® Rabbit mAb #5424
|W IF-IC||H Mk||Endogenous||160||Rabbit IgG|
Reactivity Key: H=Human Mk=Monkey
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.
Specificity / Sensitivity
MSH6 (D60G2) XP® Rabbit mAb detects endogenous levels of total MSH6 protein.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human MSH6.
Western blot analysis of extracts from various cell types using MSH6 (D60G2) XP® Rabbit mAb.
The DNA mismatch repair system (MMR) repairs post-replication DNA, inhibits recombination between nonidentical 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 MSH6 and other MMR proteins have been found in a large proportion of hereditary nonpolyposis colorectal cancer (Lynch Syndrome), the most common form of inherited colorectal cancer in the Western world (3). Mutations in MSH6 have been shown to occur in glioblastoma in response to temozolomide therapy and to promote temozolomide resistance (4).
- 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.
- Yip, S. et al. (2009) Clin Cancer Res 15, 4622-9.
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For Research Use Only. Not For Use In Diagnostic Procedures.