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Product Name
Anti-MSH2 Rabbit antibody
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Description
MSH2 Rabbit polyclonal antibody
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Tested applications
WB, IP
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Species reactivity
Human
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Alternative names
FCC1; COCA1; HNPCC; LCFS2; hMSH2; HNPCC1 antibody
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Isotype
Rabbit IgG
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Preparation
Antigen: A synthetic peptide of human MSH2
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Clonality
Polyclonal
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Formulation
Supplied in 50nM Tris-Glycine(pH 7.4), 0.15M Nacl, 40%Glycerol, 0.01% sodium azide and 0.05% BSA.
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Storage instructions
Store at -20°C. Stable for 12 months from date of receipt.
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Applications
WB: 1/1000-1/5000
IP: 1/20-1/50
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Validations
Western blot detection of MSH2 in K562,Hela cell lysates using MSH2 Rabbit pAb(1:1000 diluted).Predicted band size:105kDa.Observed band size:105kDa.
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Background
Swiss-Prot Acc.P43246.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 containg 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.
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