Mouse Anti-MSH2 Recombinant Antibody (3A2) (CBMAB-CP1584-LY)

Mouse

Human

3A2

IgG1

WB, IP, IF (ICC)

Monoclonal antibody is produced by immunizing animals with recombinant human MSH2.

Human

IgG1

Monoclonal

The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Liquid

100 µg/ml BSA, 50% glycerol

0.02% sodium azide

> 95% Purity determined by SDS-PAGE.

Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

MutS Homolog 2

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]

MutS Homolog 2; HMSH2; MutS (E. Coli) Homolog 2 (Colon Cancer; Nonpolyposis Type 1); MutS Homolog 2; Colon Cancer; Nonpolyposis Type 1 (E. Coli); MutS Homolog 2; Colon Cancer; Nonpolyposis Type 1; DNA Mismatch Repair Protein Msh2; MutS Protein Homolog 2;

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.

B cell differentiation Source: BHF-UCL
B cell mediated immunity Source: BHF-UCL
Determination of adult lifespan Source: Ensembl
DNA repair Source: BHF-UCL
Double-strand break repair Source: Ensembl
Germ cell development Source: Ensembl
Intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator Source: Ensembl
In utero embryonic development Source: Ensembl
Isotype switching Source: BHF-UCL
Maintenance of DNA repeat elements Source: HGNC-UCL
Male gonad development Source: BHF-UCL
Mismatch repair Source: UniProtKB
Mitotic intra-S DNA damage checkpoint signaling Source: Ensembl
Mitotic recombination Source: GO_Central
Negative regulation of DNA recombination Source: BHF-UCL
Negative regulation of neuron apoptotic process Source: BHF-UCL
Oxidative phosphorylation Source: Ensembl
Positive regulation of helicase activity Source: BHF-UCL
Positive regulation of isotype switching to IgA isotypes Source: Ensembl
Positive regulation of isotype switching to IgG isotypes Source: Ensembl
Postreplication repair Source: UniProtKB
Protein localization to chromatin Source: UniProtKB
Response to UV-B Source: BHF-UCL
Response to X-ray Source: BHF-UCL
Somatic hypermutation of immunoglobulin genes Source: Ensembl
Somatic recombination of immunoglobulin gene segments Source: BHF-UCL
Somatic recombination of immunoglobulin genes involved in immune response Source: GO_Central

Nucleus
Other locations
Chromosome

Hereditary non-polyposis colorectal cancer 1 (HNPCC1):
An autosomal dominant disease associated with marked increase in cancer susceptibility. It is characterized by a familial predisposition to early-onset colorectal carcinoma (CRC) and extra-colonic tumors of the gastrointestinal, urological and female reproductive tracts. HNPCC is reported to be the most common form of inherited colorectal cancer in the Western world. Clinically, HNPCC is often divided into two subgroups. Type I is characterized by hereditary predisposition to colorectal cancer, a young age of onset, and carcinoma observed in the proximal colon. Type II is characterized by increased risk for cancers in certain tissues such as the uterus, ovary, breast, stomach, small intestine, skin, and larynx in addition to the colon. Diagnosis of classical HNPCC is based on the Amsterdam criteria: 3 or more relatives affected by colorectal cancer, one a first degree relative of the other two; 2 or more generation affected; 1 or more colorectal cancers presenting before 50 years of age; exclusion of hereditary polyposis syndromes. The term 'suspected HNPCC' or 'incomplete HNPCC' can be used to describe families who do not or only partially fulfill the Amsterdam criteria, but in whom a genetic basis for colon cancer is strongly suspected.
Muir-Torre syndrome (MRTES):
Rare autosomal dominant disorder characterized by sebaceous neoplasms and visceral malignancy.
Endometrial cancer (ENDMC):
A malignancy of endometrium, the mucous lining of the uterus. Most endometrial cancers are adenocarcinomas, cancers that begin in cells that make and release mucus and other fluids.
Mismatch repair cancer syndrome 2 (MMRCS2):
An autosomal recessive form of mismatch repair cancer syndrome, a childhood cancer predisposition syndrome encompassing a broad tumor spectrum. This includes hematological malignancies, central nervous system tumors, Lynch syndrome-associated malignancies such as colorectal tumors as well as multiple intestinal polyps, embryonic tumors and rhabdomyosarcoma. Multiple cafe-au-lait macules, a feature reminiscent of neurofibromatosis type 1, are often found as first manifestation of the underlying cancer.
Colorectal cancer (CRC):
A complex disease characterized by malignant lesions arising from the inner wall of the large intestine (the colon) and the rectum. Genetic alterations are often associated with progression from premalignant lesion (adenoma) to invasive adenocarcinoma. Risk factors for cancer of the colon and rectum include colon polyps, long-standing ulcerative colitis, and genetic family history.

Phosphorylated by PRKCZ, which may prevent MutS alpha degradation by the ubiquitin-proteasome pathway.