Anti-MSH2 (aa 875-934) polyclonal antibody

Antibody Isotype

IgG

Species Reactivity

Mouse; Human

Immunogen

Synthetic peptide: LEREQGEKII QEFLSKVKQM PFTEMSEENI TIKLKQLKAE VIAKNNSFVN EIISRIKVTT, corresponding to C terminal amino acids 875-934 of Human MSH2

Conjugate

Application Notes

ICC/IF: 1 μg/ml; WB: 1/5000 - 1/15000; IP: 2-5 μg/mg; IHC-P: 1/1000 - 1/5000.

Alternative Names

MSH2; mutS homolog 2, colon cancer, nonpolyposis type 1 (E. coli); COCA1, mutS (E. coli) homolog 2 (colon cancer, nonpolyposis type 1); DNA mismatch repair protein Msh2; HNPCC; HNPCC1; hMSH2; FCC1; COCA1; LCFS2;

Entrez Gene ID

UniProt ID

Antigen Description

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. 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.

Pathway

BRCA1-associated genome surveillance complex (BASC); Colorectal cancer; Direct p53 effectors; Mismatch repair; Pathways in cancer;