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.
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注意事项：
1.Since applications vary, each investigator should titrate the reagent to obtain optimal results.
2.Caution: Sodium azide yields highly toxic hydrazoic acid under acidic conditions. Dilute azide compounds in running water before discarding to avoid accumulation of potentially explosive deposits in plumbing.
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