M
Mitch McVey
Researcher at Tufts University
Publications - 53
Citations - 5952
Mitch McVey is an academic researcher from Tufts University. The author has contributed to research in topics: DNA repair & Homologous recombination. The author has an hindex of 25, co-authored 46 publications receiving 5418 citations. Previous affiliations of Mitch McVey include University of North Carolina at Chapel Hill & Massachusetts Institute of Technology.
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The SIR2/3/4 complex and SIR2 alone promote longevity in Saccharomyces cerevisiae by two different mechanisms
TL;DR: It is shown that life span regulation by the Sir proteins is independent of their role in nonhomologous end joining, and increasing the gene dosage extends the life span in wild-type cells.
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MMEJ repair of double-strand breaks (director’s cut): deleted sequences and alternative endings
Mitch McVey,Sang Eun Lee +1 more
TL;DR: A mechanistic model for MMEJ is proposed and important questions for future research are highlighted, including how microhomology contributes to oncogenic chromosome rearrangements and genetic variation in humans.
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Error-Prone Repair of DNA Double-Strand Breaks.
Kasey Rodgers,Mitch McVey +1 more
TL;DR: This review describes the two major strategies used to repair double strand breaks: non‐homologous end joining and homologous recombination, emphasizing the mutagenic aspects of each.
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The Saccharomyces cerevisiae WRN homolog Sgs1p participates in telomere maintenance in cells lacking telomerase
F. Brad Johnson,F. Brad Johnson,F. Brad Johnson,Robert A. Marciniak,Robert A. Marciniak,Mitch McVey,Sheila A. Stewart,William C. Hahn,William C. Hahn,William C. Hahn,Leonard Guarente +10 more
TL;DR: It is shown that WRN co‐localizes with telomeric factors in telomerase‐independent immortalized human cells, and further that the budding yeast RecQ family helicase Sgs1p influences telomere metabolism in yeast cells lacking telomersase.
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Drosophila BLM in double-strand break repair by synthesis-dependent strand annealing.
TL;DR: In this article, it was shown that mutants of the RecQ DNA helicase gene are severely impaired in their ability to carry out repair DNA synthesis during synthesis-dependent strand annealing, and that repair in the mutants is completed by error-prone pathways that create large deletions.