Product Detail
Product NameMSH2 Antibody HRP Conjugated
Host SpeciesRabbit
ClonalityPolyclonal
IsotypeIgG
PurificationPurified by Protein A.
ApplicationsWB IHC-F
Species ReactivityHu Ms
Immunogen DescKLH conjugated synthetic peptide aa 80-130 935 derived from human MSH-2
Target NameMSH2
ConjugateHRP
Excitation EmissionN A
Other NamesFCC1; COCA1; HNPCC; LCFS2; HNPCC1; DNA mismatch repair protein Msh2; hMSH2; MutS protein homolog 2; MSH2
Accession NoSwiss-Prot#P43246
NCBI Gene ID4436
Uniprot
P43246
Gene ID
4436;
Concentration1mg ml
Formulation0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
StorageShipped at 4˚C. Store at -20˚C for one year. Avoid repeated freeze/thaw cycles.
Application Details
WB=1:500-2000 IHC-F=1:50-200
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.
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