MSH6 Mouse, Unlabeled, Clone: 44, BD

Description

• 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
• Immunofluorescence, Western Blotting