Anti-PMS2 Antibody (aa623-639, clone 163C1251) IHC-plus; PMS2; HNPCC4; H_DJ0042M02.9; PMS2CL; PMSL2; PMS1 protein homolog 2; Human PMS2

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

Monoclonal

IgG1

163C1251

Mouse

A synthetic peptide corresponding to amino acids 623-639 SSLAKRIKQLHHEAQQS of human PMS2; GenBank No. NP_000526.1.

Protein G Purified

PBS, 0.02% sodium azide.

0.5 mg/ml (lot specific)

Short term 4 degree C, long term aliquot and store at -20 degree C, avoid freeze thaw cycles.

Small volumes of anti-PMS2 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.

Immunohistochemistry (IHC - Paraffin), Western Blot (WB)

IHC-P (5 ug/ml), WB (1 - 2 ug/ml)
Usage: Immunohistochemistry: was validated for use in immunohistochemistry on a panel of 21 formalin-fixed, paraffin-embedded (FFPE) human tissues after heat induced antigen retrieval in pH 6.0 citrate buffer. After incubation with the primary anti...

Anti-PMS2 antibody IHC of human breast. Immunohistochemistry of formalin-fixed, paraffin-embedded tissue after heat-induced antigen retrieval. Antibody concentration 5 ug/ml.

Western blot of PMS2 using antibody at 2 ug/ml against 10 ug of NIH 3T3 cell lysate.

20,073 Da

PMS2 postmeiotic segregation increased 2 (S. cerevisiae)

mismatch repair endonuclease PMS2; H_DJ0042M02.9; PMS1 protein homolog 2; DNA mismatch repair protein PMS2

Mismatch repair endonuclease PMS2

PMSL2??[Similar Products]

PMS2_HUMAN

This gene is one of the PMS2 gene family members found in clusters on chromosome 7. The product of this gene is involved in DNA mismatch repair. It forms a heterodimer with MLH1 and this complex interacts with other complexes bound to mismatched bases. Mutations in this gene are associated with hereditary nonpolyposis colorectal cancer, Turcot syndrome, and are a cause of supratentorial primitive neuroectodermal tumors. Alternatively spliced transcript variants have been observed for this gene. [provided by RefSeq, Jul 2008]

PMS2: Component of the post-replicative DNA mismatch repair system (MMR). Heterodimerizes with MLH1 to form MutL alpha. DNA repair is initiated by MutS alpha (MSH2-MSH6) or MutS beta (MSH2- MSH6) binding to a dsDNA mismatch, then MutL alpha is recruited to the heteroduplex. Assembly of the MutL-MutS-heteroduplex ternary complex in presence of RFC and PCNA is sufficient to activate endonuclease activity of PMS2. It introduces single-strand breaks near the mismatch and thus generates new entry points for the exonuclease EXO1 to degrade the strand containing the mismatch. DNA methylation would prevent cleavage and therefore assure that only the newly mutated DNA strand is going to be corrected. MulL alpha (MLH1-PMS2) interacts physically with the clamp loader subunits of DNA polymerase III, suggesting that it may play a role to recruit the DNA polymerase III to the site of the MMR. Also implicated in DNA damage signaling, a process which induces cell cycle arrest and can lead to apoptosis in case of major DNA damages. Defects in PMS2 are the cause of hereditary non-polyposis colorectal cancer type 4 (HNPCC4). Mutations in more than one gene locus can be involved alone or in combination in the production of the HNPCC phenotype (also called Lynch syndrome). Most families with clinically recognized HNPCC have mutations in either MLH1 or MSH2 genes. HNPCC is an autosomal, dominantly inherited disease associated with marked increase in cancer susceptibility. It is characterized by a familial predisposition to early onset colorectal carcinoma (CRC) and extra-colonic cancers 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, and accounts for 15% of all colon cancers. Cancers in HNPCC originate within benign neoplastic polyps termed adenomas. Clinically, HNPCC is often divided into two subgroups. Type I: hereditary predisposition to colorectal cancer, a young age of onset, and carcinoma observed in the proximal colon. Type II: patients have an 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. Defects in PMS2 are a cause of mismatch repair cancer syndrome (MMRCS); also known as Turcot syndrome or brain tumor-polyposis syndrome 1 (BTPS1). MMRCS is an autosomal dominant disorder characterized by malignant tumors of the brain associated with multiple colorectal adenomas. Skin features include sebaceous cysts, hyperpigmented and cafe au lait spots. Belongs to the DNA mismatch repair MutL/HexB family. 4 isoforms of the human protein are produced by alternative splicing.

Protein type: Hydrolase; EC 3.1.-.-; DNA repair, damage; Cell cycle regulation; Tumor suppressor

Chromosomal Location of Human Ortholog: 7p22.2

Cellular Component: MutLalpha complex; nucleoplasm; microtubule cytoskeleton; cytoplasm; nucleus

Molecular Function: protein binding; single base insertion or deletion binding; DNA binding; endonuclease activity; ATPase activity; MutSalpha complex binding; single-stranded DNA binding; ATP binding

Biological Process: response to drug; mismatch repair; somatic hypermutation of immunoglobulin genes; somatic recombination of immunoglobulin gene segments; DNA repair

Disease: Colorectal Cancer, Hereditary Nonpolyposis, Type 4; Mismatch Repair Cancer Syndrome

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