Anti-MutS Protein Homolog 2(MSH2), clone YN01126m

DNA mismatch repair (MMR) system is composed of enzyme molecules that specifically repair DNA base mismatch. The existence of this system can ensure the integrity and stability of genetic material, avoid the mutation of genetic material, and ensure the high fidelity of DNA replication. It is composed of hMLH1, hMSH2, hpms1, hPMS2 and other genes. HMSH2 is located in human chromosome 2p21-22, encoding a protein composed of 934 aa. The mutation of hMSH2 gene occurs in sporadic colorectal cancer. The mutation of microsatellite hMSH2 gene is related to 50% of familial and non-familial polyposis colorectal cancer (HNPCC). 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]