PMS2 sirna

PMS2 siRNA (Human)

Cat. Num. AAA8212154

• Gene Names: PMS2; MLH4; PMSL2; HNPCC4; PMS2CL
• Reactivity: Human
• Applications: RNA Interference (RNAi)
• Purity: > 97%
• Synonyms: PMS2; PMS2 siRNA (Human); PMSL2; Mismatch repair endonuclease PMS2; DNA mismatch repair protein PMS2; PMS1 protein homolog 2; PMS2 sirna

• Host: Synthetic
• Reactivity: Human
• Specificity: PMS2 siRNA (Human) is a target-specific 19-23 nt siRNA oligo duplexes designed to knock down gene expression.
• Purity/Purification: > 97%
• Form/Format: Lyophilized powder
• Sequence Length: 862

• Applicable Applications for PMS2 sirna: RNA Interference (RNAi)
• Quality Control: Oligonucleotide synthesis is monitored base by base through trityl analysis to ensure appropriate coupling efficiency. The oligo is subsequently purified by affinity-solid phase extraction. The annealed RNA duplex is further analyzed by mass spectrometry to verify the exact composition of the duplex. Each lot is compared to the previous lot by mass spectrometry to ensure maximum lot-to-lot consistency.
• Directions for Use: We recommends transfection with 100 nM siRNA 48 to 72 hours prior to cell lysis. Before resuspending, briefly centrifuge the tube to ensure the lyophilized siRNA is at the bottom of the tube. Resuspend the siRNA oligos to an appropriate concentration with DEPC water. For each vial, suitable for 250 transfections in 24 well plate (20 pmol for each well).
• Components: We offer pre-designed sets of 3 different target-specific siRNA oligo duplexes of human PMS2 gene. Each vial contains 5 nmol of lyophilized siRNA. The duplexes can be transfected individually or pooled together to achieve knockdown of the target gene, which is most commonly assessed by qPCR or western blot. Our siRNA oligos are also chemically modified (2'-OMe) at no extra charge for increased stability and enhanced knockdown in vitro and in vivo.
• Preparation and Storage: Shipped at 4 degree C. Store at -20 degree C for one year.

Related Product Information for PMS2 sirna

siRNA to inhibit PMS2 expression using RNA interference

NCBI and Uniprot Product Information

• NCBI GI #: 4505913
• NCBI GeneID: 5395
• NCBI Accession #: NP_000526.1
• NCBI GenBank Nucleotide #: NM_000535.5
• UniProt Accession #: P54278; Q52LH6; Q5FBW9; Q5FBX1; Q5FBX2; Q75MR2; B2R610
• Molecular Weight: 20,073 Da
• NCBI Official Full Name: mismatch repair endonuclease PMS2 isoform a
• NCBI Official Synonym Full Names: PMS1 homolog 2, mismatch repair system component
• NCBI Official Symbol: PMS2
• NCBI Official Synonym Symbols: MLH4; PMSL2; HNPCC4; PMS2CL
• NCBI Protein Information: mismatch repair endonuclease PMS2
• UniProt Protein Name: Mismatch repair endonuclease PMS2
• Protein Family: Mismatch repair endonuclease
• UniProt Gene Name: PMS2
• UniProt Synonym Gene Names: PMSL2
• UniProt Entry Name: PMS2_HUMAN

NCBI Description

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]

Uniprot Description

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

Chromosomal Location of Human Ortholog: 7p22.2

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

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