Isolated short CTG/CAG DNA slip-outs are repaired efficiently by hMutSbeta, but clustered slip-outs are poorly repaired.
|Abstract||Expansions of CTG/CAG trinucleotide repeats, thought to involve slipped DNAs at the repeats, cause numerous diseases including myotonic dystrophy and Huntington's disease. By unknown mechanisms, further repeat expansions in transgenic mice carrying expanded CTG/CAG tracts require the mismatch repair (MMR) proteins MSH2 and MSH3, forming the MutSbeta complex. Using an in vitro repair assay, we investigated the effect of slip-out size, with lengths ... [truncated at 450 characters in length]|
|Author||Panigrahi, Gagan B; Slean, Meghan M; Simard, Jodie P; et al|
|Subject||Animals Cluster Analysis DNA DNA Mismatch Repair Humans Mice Mice, Transgenic Mutation Myotonic Dystrophy Proteins Trinucleotide Repeats genetics metabolism genetics genetics genetics|