Product Pathways - DNA Damage
MSH2 (3A2) Mouse mAb #2850
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PhosphoSitePlus® protein, site, and accession data: MSH2
| Applications | Reactivity | Sensitivity | MW (kDa) | Isotype |
|---|---|---|---|---|
| W IP IF-IC | H | Endogenous | 100 | Mouse IgG1 |
Applications Key:
W=Western Blotting
IP=Immunoprecipitation
IF-IC=Immunofluorescence (Immunocytochemistry)
Reactivity Key:
H=Human
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.
Protocols
Specificity / Sensitivity
MSH2 (3A2) Mouse mAb detects endogenous levels of total MSH2 protein.
Source / Purification
Monoclonal antibody is produced by immunizing animals with recombinant human MSH2.
Western Blotting
Western blot analysis of extracts of HeLa and OVCAR3 cells using MSH2 (3A2) Mouse mAb.
IF-IC
Confocal immunofluorescent analysis of HeLa cells using MSH2 (3A2) Mouse mAb (green). Actin filaments have been labeled with DY554 phalloidin (red).
Background
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.
Application References
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For Research Use Only. Not For Use In Diagnostic Procedures.
