MSH6 Pure 44/MSH6 50ug

DNA mismatch repair in bacteria is carried out by the MutL, MutH, and MutS proteins. Initial binding of MutS to the mismatched DNA is

followed by binding of the MutH endonuclease and MutL. Together these proteins form a complex that mediates excision repair. Mutations or

deficiencies of any of these bacterial proteins results in a mutator phenotype that is characterized by genetic instability. MSH2, MSH3, and

MSH6 are human homologs of MutS, while MLH1, PMS1, and PMS2 are homologs of MutL. As a heterodimer with MSH2, MSH6 binds to

DNA containing G/T mismatches. The MSH2-MSH6 complex recognizes single-base mispairs and insertion/deletion loops. Binding of this

complex induces conformational changes in the DNA that lead to the binding of an MLH-PMS1 complex and excision repair. Mutations in the

human genes are associated with hereditary nonpolyposis colon cancer (HNPCC), a common hereditary disease in humans. HNPCC is

characterized by frequent microsatellite mutations that arise from somatic mutation due to a replication error (RER+) phenotype. This

phenotype is analogous to the bacterial system and is directly linked to DNA mismatch repair deficiencies.

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.