MSH3 Mouse anti-Human, Unlabeled, Clone: 52, BD
Mouse Monoclonal Antibody
Supplier: BD Biosciences 611390
Bacterial mismatch DNA repair involves the MutL, MutH, and MutS proteins, which forms a complex that mediates excision repair. Mutations in or deficiencies of any of these proteins results in a mutator phenotype that is characterized by genetic instability. Human homologs of MutS include MSH2, MSH3, and MSH6. MSH2 forms heterodimers with MSH6 (hMutSα) or MSH3 (hMutSβ) that specifically bind single-mispaired nucleotides and a subset of insertion-deletion mismatches. In addition, these heterodimers have intrinsic ATPase activity that is regulated by mismatch binding. ADP-bound heterodimers bind mismatched nucleotides, while ATP-bound heterodimers do not. The role of MSH3 in genetic stability in human cells in unclear. However, MSH3 and MSH6 share roles in the control of mutation rates. Both participate in repair of replication errors containing base-base mismatches or 1-4 extra bases. The MSH3 gene is located upstream of the dihydrofolate reductase (DHFR) gene and is expressed at low levels in a variety of human tissues. Thus, MSH3 is a component of an adenosine nucleotide-regulated molecular switch whose activity is essential for classical nucleotide mismatch repair.
Immunofluorescence, Western Blotting
|Aqueous buffered solution containing BSA, glycerol, and ≤0.09% sodium azide.|
|Human MSH3 aa. 136-349|
|Store undiluted at -20°C.|
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