MSH2, Polyclonal Antibody

HNPCC; COCA1; Flow cytometryC1; HNPCC1; BAT-26; Familial Nonpolyposis Colon Cancer Type 1; Colorectal Cancer Type 1

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

Polyclonal

IgG

Rabbit

Affinity purified

100 ug (0.2 mg/ml) purified rabbit polyclonal antibody in phosphate-buffered saline (PBS) containing 50% glycerol, 1% BSA, and 0.02% sodium azide.
Appearance: Colorless liquid

0.2 mg/ml (lot specific)

At -20 degree C
Shelf Life: 12 months

Small volumes of anti-MSH2 antibody 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.

Background: DNA mismatch repair genes have been found to be associated with hereditary nonpolyposis colorectal cancer (HNPCC). Inherited mutations in the MSH2 were demonstrated at high frequency in HNPCC and were shown to be associated with microsatellite instability. The demonstration that 10 to 45% of pancreatic, gastric, breast, ovarian and small cell lung cancers also display microsatellite instability smuggests that DNA mismatch repair is not restricted to HNPCC tumors but is a common feature in tumor initiation or progression.

Western Blot (WB), Immunoprecipitation (IP), Immunofluorescence (IF), Immunohistochemistry (IHC)

Western blotting (1-4 ug/ml), immunoprecipitation (15-25 ug/ml), and Immunohistochemistry (15-25 ug/ml). However, the optimal concentrations should be determined individually. The antibody recognizes the MSH2 of human, mouse, and rat origins. Reactivity to other species has not been tested.

97,323 Da

mutS homolog 2

DNA mismatch repair protein Msh2

DNA mismatch repair protein Msh2

hMSH2  [Similar Products]

MSH2_HUMAN

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]

MSH2: 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. Heterodimer consisting of MSH2-MSH6 (MutS alpha) or MSH2- MSH3 (MutS beta). Both heterodimer form a ternary complex with MutL alpha (MLH1-PMS1). Interacts with EXO1. Part of the BRCA1- associated genome surveillance complex (BASC), which contains BRCA1, MSH2, MSH6, MLH1, ATM, BLM, PMS2 and the RAD50-MRE11-NBS1 protein complex. This association could be a dynamic process changing throughout the cell cycle and within subnuclear domains. Interacts with ATR. Interacts with SLX4/BTBD12; this interaction is direct and links MutS beta to SLX4, a subunit of different structure-specific endonucleases. Interacts with SMARCAD1. Ubiquitously expressed. Belongs to the DNA mismatch repair MutS family.

Protein type: DNA-binding; Tumor suppressor

Chromosomal Location of Human Ortholog: 2p21

Cellular Component: nucleoplasm; nuclear chromosome; membrane; MutSalpha complex; MutSbeta complex

Molecular Function: protein C-terminus binding; DNA-dependent ATPase activity; protein homodimerization activity; double-strand/single-strand DNA junction binding; dinucleotide repeat insertion binding; single thymine insertion binding; ATPase activity; oxidized purine DNA binding; magnesium ion binding; ADP binding; protein kinase binding; mismatched DNA binding; loop DNA binding; centromeric DNA binding; Y-form DNA binding; protein binding; enzyme binding; DNA binding; four-way junction DNA binding; single guanine insertion binding; guanine/thymine mispair binding; double-stranded DNA binding; MutLalpha complex binding; dinucleotide insertion or deletion binding; ATP binding; single-stranded DNA binding

Biological Process: determination of ***** life span; maintenance of DNA repeat elements; germ cell development; positive regulation of helicase activity; double-strand break repair; negative regulation of neuron apoptosis; cell cycle arrest; DNA damage response, signal transduction by p53 class mediator resulting in induction of apoptosis; response to X-ray; oxidative phosphorylation; negative regulation of DNA recombination; mismatch repair; in utero embryonic development; postreplication repair; male gonad development; somatic hypermutation of immunoglobulin genes; isotype switching; DNA repair; response to UV-B; meiotic mismatch repair; B cell mediated immunity; intra-S DNA damage checkpoint; B cell differentiation; meiotic gene conversion; somatic recombination of immunoglobulin gene segments; negative regulation of meiotic recombination

Disease: Muir-torre Syndrome; Mismatch Repair Cancer Syndrome; Lynch Syndrome I

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