作者: David A. Boothman , Carmell Wilson-Van Patten , Samir Acharya , Teresa Wilson , Eric Odegaard
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摘要: Abstract Hereditary nonpolyposis colorectal cancer is a susceptibility syndrome that has been found to be caused by mutations in any of several genes involved DNA mismatch repair, including hMSH2, hMLH1, or hPMS2. Recent reports have suggested hMSH2 and hMLH1 role the regulation cell cycle. To determine if these are cycle regulated, we examined their mRNA protein levels throughout IMR-90 normal human lung fibroblasts. We demonstrate do not change appreciably Although remained constant, there was modest (approximately 50%) increase its during late G1 S phase. The hPMS2 fluctuated (decreasing 50% increasing phase), whereas increased Our data indicate that, at least cells, machinery responsible for detection repair mismatched bases present