DNA damage, if not repaired, can become a mutation. Mutation
accumulation is associated with initiation and progression of tumorigenesis. DNA
mismatch repair (MMR) is required for maintaining genetic stability by repairing
replication errors. Biochemical studies have shown that MMR also recognizes
mismatch-causing DNA lesions, suggesting the role of MMR in...
Mismatch repair is one of the mechanisms by which cells ensure genomic
stability. Deficiencies in mismatch repair (MMR) increase mutation rates and cancer
risks. In the well-characterized methyl-directed Escherichia co/i system, MMR is
initiated by MutS, Mut L, and MutH proteins. The single MutS protein and the
single MutL protein...
The DNA mismatch repair (MMR) pathway maintains genomic stability and
reduces cancer risk (colorectal and other internal cancers) by correcting polymerase
errors and activating cell cycle checkpoints and apoptosis in response to DNA damage.
Few studies have examined the influence of commonly encountered environmental
mutagens/carcinogens on the etiology of MMR-deficient...
Escherichia coli double-strand uracil-DNA glycosylase (Dug) was purified to apparent homogeneity from bacteria that were defective in uracil-DNA glycosylase (Ung). After cloning the dug gene, recombinant Dug was overexpressed, purified, and characterized with respect to activity, substrate specificity, product DNA binding, and mechanism of action. Purified Dug excised both uracil...