Anti-MSH2 monoclonal antibody, clone FQS4055 Knockout Validated

Antibody Isotype

IgG

Clone

FQS4055

Species Reactivity

Human

Immunogen

Synthetic peptide (the amino acid sequence is considered to be commercially sensitive)

Conjugate

Application Notes

WB: 1/1000 - 1/10000; IP: 1/10 - 1/100;

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), organism-specific biosystem; Colorectal cancer, organism-specific biosystem; Colorectal cancer, conserved biosystem; Direct p53 effectors, organism-specific biosystem; Mismatch repair, organism-specific biosystem; Mismatch repair, conserved biosystem; Pathways in cancer, organism-specific biosystem;