Anti-MSH2 Rabbit (Clone RM478)

MutS homolog 2 (MSH2) is a DNA repair protein. It heterodimerizes with MSH6 or MSH3 to form the MutSalpha and MutSbeta DNA mismatch recognition complexes, respectively, which are divided into five domains: a mismatch-binding domain, connector domain, alpha-helical lever domain, clamp domain, and an ABC-ATPase domain. It is ubiquitously expressed and localized to the nucleus. MSH2, when complexed with MSH6 or MSH3, recognizes DNA polymerase errors in replicated DNA to activate MutL and initiate DNA repair. Missense mutations in MSH2 are associated with hereditary nonpolyposis colorectal cancer (HNPCC). Polymorphisms in MSH2 are associated with an increased risk of developing prostate cancer. Cayman's MSH2 Rabbit Monoclonal Antibody (Clone RM478) can be used for immunohistochemistry (IHC) and Western blot (WB) applications.. Cross reactivity: (+) MSH2: . (+) Human: .. Protein function: Component of the post-replicative DNA mismatch repair system (MMR). Forms two different heterodimers: MutS alpha (MSH2-MSH6 heterodimer) and MutS beta (MSH2-MSH3 heterodimer) which binds to DNA mismatches thereby initiating DNA repair. When bound, heterodimers bend the DNA helix and shields approximately 20 base pairs. MutS alpha recognizes single base mismatches and dinucleotide insertion-deletion loops (IDL) in the DNA. MutS beta recognizes larger insertion-deletion loops up to 13 nucleotides long. After mismatch binding, MutS alpha or beta forms a ternary complex with the MutL alpha heterodimer, which is thought to be responsible for directing the downstream MMR events, including strand discrimination, excision, and resynthesis. Recruits DNA helicase MCM9 to chromatin which unwinds the mismatch containing DNA strand (PubMed:26300262). ATP binding and hydrolysis play a pivotal role in mismatch repair functions. The ATPase activity associated with MutS alpha regulates binding similar to a molecular switch: mismatched DNA provokes ADP-->ATP exchange, resulting in a discernible conformational transition that converts MutS alpha into a sliding clamp capable of hydrolysis-independent diffusion along the DNA backbone. This transition is crucial for mismatch repair. MutS alpha may also play a role in DNA homologous recombination repair. In melanocytes may modulate both UV-B-induced cell cycle regulation and apoptosis. [The UniProt Consortium]