MSH2 sirna

MSH2 siRNA (Mouse)

Cat. Num. AAA8228025

• Gene Names: Msh2; AI788990
• Reactivity: Mouse
• Applications: RNA Interference (RNAi)
• Purity: > 97%
• Synonyms: MSH2; MSH2 siRNA (Mouse); DNA mismatch repair protein Msh2; MutS protein homolog 2; MSH2 sirna

• Host: Synthetic
• Reactivity: Mouse
• Specificity: MSH2 siRNA (Mouse) 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: 935

• Applicable Applications for MSH2 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 mouse MSH2 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 MSH2 sirna

siRNA to inhibit MSH2 expression using RNA interference

NCBI and Uniprot Product Information

• NCBI GI #: 6678938
• NCBI GeneID: 17685
• NCBI Accession #: NP_032654.1
• NCBI GenBank Nucleotide #: NM_008628.2
• UniProt Accession #: P43247
• Molecular Weight: 104,151 Da
• NCBI Official Full Name: DNA mismatch repair protein Msh2
• NCBI Official Synonym Full Names: mutS homolog 2 (E. coli)
• NCBI Official Symbol: Msh2
• NCBI Official Synonym Symbols: AI788990
• NCBI Protein Information: DNA mismatch repair protein Msh2
• UniProt Protein Name: DNA mismatch repair protein Msh2
• Protein Family: DNA mismatch repair protein
• UniProt Gene Name: Msh2
• UniProt Entry Name: MSH2_MOUSE

Uniprot Description

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

Cellular Component: nuclear chromosome; membrane; MutSalpha complex; intracellular; nucleus; MutSbeta complex

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

Biological Process: somatic recombination of immunoglobulin genes during immune response; determination of adult 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; oxidative phosphorylation; response to X-ray; negative regulation of DNA recombination; mismatch repair; in utero embryonic development; postreplication repair; male gonad development; somatic hypermutation of immunoglobulin genes; isotype switching; cell cycle; DNA repair; meiotic mismatch repair; response to UV-B; B cell mediated immunity; DNA damage response, signal transduction resulting in induction of apoptosis; intra-S DNA damage checkpoint; B cell differentiation; somatic recombination of immunoglobulin gene segments; meiotic gene conversion; response to DNA damage stimulus; negative regulation of meiotic recombination