COCA1; FCC1; HNPCC; HNPCC1; LCFS2; mutS homolog 2

For Research Use Only. Not for use in diagnostic procedures.

This assay has high sensitivity and excellent specificity for detection of Human MSH2. No significant cross-reactivity or interference between Human MSH2 and analogues was observed.

Store at 2-8 degree C.

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Small volumes of MSH2 elisa kit vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

MBS287532 is a ready-to-use microwell, strip plate ELISA (enzyme-linked immunosorbent assay) Kit for analyzing the presence of the DNA mismatch repair protein Msh2 (MSH2) ELISA Kit target analytes in biological samples. The concentration gradients of the kit standards or positive controls render a theoretical kit detection range in biological research samples containing MSH2. The ELISA analytical biochemical technique of the MBS287532 kit is based on MSH2 antibody-MSH2 antigen interactions (immunosorbency) and an HRP colorimetric detection system to detect MSH2 antigen targets in samples. The ELISA Kit is designed to detect native, not recombinant, MSH2. Appropriate sample types may include undiluted body fluids and/or tissue homogenates, secretions. Quality control assays assessing reproducibility identified the intra-assay CV (%) and inter-assay CV(%).

Description: This assay employs a two-site sandwich ELISA to quantitate MSH2 in samples. An antibody specific for MSH2 has been pre-coated onto a microplate. Standards and samples are pipetted into the wells and any MSH2 present is bound by the immobilized antibody. After removing any unbound substances, a biotin-conjugated antibody specific for MSH2 is added to the wells. After washing, Streptavidin conjugated Horseradish Peroxidase (HRP) is added to the wells. Following a wash to remove any unbound avidin-enzyme reagent, a substrate solution is added to the wells and color develops in proportion to the amount of MSH2 bound in the initial step. The color development is stopped and the intensity of the color is measured.
Overview: MSH2 was identified as a locus frequently mutated in hereditary nonpolyposis colon cancer (HNPCC). When cloned, it was discovered to be a human homolog of the E. coli mismatch repair gene mutS, consistent with the characteristic alterations in microsatellite sequences (RER+ phenotype) found in HNPCC. It is also associated with some endometrial cancers.
MSH2 is homologous to a prokaryotic gene, MutS, that participates in mismatch repair. The highest homology is to the yeast Msh2 gene in the helix-turn-helix domain, perhaps responsible for MutS binding to DNA. The yeast and human Msh2 proteins are 77% identical between codons 615 and 788. There are 10 other blocks of similar amino acids distributed throughout the length of the 2 proteins.

97,323 Da

mutS homolog 2

DNA mismatch repair protein Msh2

DNA mismatch repair protein Msh2

hMSH2??[Similar Products]

This locus is frequently mutated in hereditary nonpolyposis colon cancer (HNPCC). When cloned, it was discovered to be a human homolog of the E. coli mismatch repair gene mutS, consistent with the characteristic alterations in microsatellite sequences (RER+ phenotype) found in HNPCC. Two transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Apr 2012]

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.

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