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David C. Thomas

Researcher at National Institutes of Health

Publications -  19
Citations -  1799

David C. Thomas is an academic researcher from National Institutes of Health. The author has contributed to research in topics: DNA replication & DNA. The author has an hindex of 16, co-authored 19 publications receiving 1759 citations. Previous affiliations of David C. Thomas include Research Triangle Park.

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Requirement for PCNA in DNA mismatch repair at a step preceding DNA resynthesis

TL;DR: The data suggest a PCNA requirement in mismatch repair at a step preceding DNA resynthesis in yeast and human expression libraries, and the ability of PCNA to bind to MLH1 and MSH2 may reflect linkage between mismatch repair and replication.
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Heteroduplex repair in extracts of human HeLa cells

TL;DR: Parallel measurements of repair in HeLa extracts and in Escherichia coli suggest that repair specificities are similar for the two systems, and suggests that DNA polymerase alpha may function in mismatch repair.
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Defective mismatch repair in extracts of colorectal and endometrial cancer cell lines exhibiting microsatellite instability.

TL;DR: In this paper, the authors compared cell-free extracts from RER+ endometrial and colorectal cancer cell lines to RER- cell lines, and found that the defect in these lines likely involves pre-incision events or the excision step, but not the incision, polymerization, or ligation steps.
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Fidelity of mammalian DNA replication and replicative DNA polymerases.

TL;DR: The fidelity of SV40 origin-dependent DNA replication in human cell extracts is compared to the fidelity of mammalian DNA polymerases alpha, delta, and epsilon using lacZ alpha of M13mp2 as a reporter gene to demonstrate that exonucleolytic proofreading contributes to accuracy during synthesis by DNA polymerase delta.
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Replication of UV-irradiated DNA in human cell extracts: Evidence for mutagenic bypass of pyrimidine dimers

TL;DR: Sequence analysis of mutants resulting from replication of UV-irradiated DNA demonstrated that most mutants contained C-->T transition errors at dipyrimidine sites, consistent with the interpretation that pyrimidine dimers are bypassed during replication by the multiprotein replication apparatus in human cell extracts.