Article
Structure-forming CAG/CTG repeat sequences are sensitive to breakage in the absence of Mrc1 checkpoint function and S-phase checkpoint signaling: implications for trinucleotide repeat expansion diseases.
Cell cycle (Georgetown, Tex.) - 1 Nov 2004
Freudenreich Catherine H, Lahiri Mayurika
Abstract excerpt
Expansion of trinucleotide repeat sequences is the cause of multiple inherited human genetic diseases including Huntington's disease and myotonic dystrophy. CTG and CAG repeats have been shown to form stable secondary structures that can impair Okazaki fragment processing and may impede replication fork progression. We recently showed that mutation of DNA damage checkpoint proteins results in increased chromosome...
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