MSH3 Mouse anti-Human, Unlabeled, Clone: 52, BD

Description

• 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