J
Jac A. Nickoloff
Researcher at Colorado State University
Publications - 64
Citations - 5082
Jac A. Nickoloff is an academic researcher from Colorado State University. The author has contributed to research in topics: DNA repair & Homologous recombination. The author has an hindex of 33, co-authored 60 publications receiving 4736 citations. Previous affiliations of Jac A. Nickoloff include University of Illinois at Chicago & University of New Mexico.
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Regulation of DNA double-strand break repair pathway choice
TL;DR: The regulatory factors that regulate DSB repair by NHEJ and HR in yeast and higher eukaryotes are reviewed, including regulated expression and phosphorylation of repair proteins, chromatin modulation of repair factor accessibility, and the availability of homologous repair templates.
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Chromatin remodelling at a DNA double-strand break site in Saccharomyces cerevisiae
TL;DR: It is shown that near a DSB phosphorylation of H2A is followed by loss of histones H2B and H3 and increased sensitivity of chromatin to digestion by micrococcal nuclease, which indicates that MRX-dependent nucleosome remodelling regulates the accessibility of factors directly involved in DNA repair by homologous recombination.
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Gene conversion tracts from double-strand break repair in mammalian cells
TL;DR: The results suggest that chromosome ends in mammalian cells are generally protected from extensive degradation prior to recombination, and heterology decreases the efficiency of recombinational repair.
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A YY1–INO80 complex regulates genomic stability through homologous recombination–based repair
Su Wu,Yujiang Shi,Yujiang Shi,Peter Mulligan,Joseph Landry,Huifei Liu,Ju Lu,Hank H. Qi,Weijia Wang,Jac A. Nickoloff,Carl Wu,Yang Shi +11 more
TL;DR: Functional assays revealed that both YY1 and INO80 are essential in homologous recombination–based DNA repair (HRR), which was further supported by the finding that YY 1 preferentially bound a recombination-intermediate structure in vitro.
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DNA-dependent protein kinase suppresses double-strand break-induced and spontaneous homologous recombination.
TL;DR: DNA-PKcs may suppress spontaneous HR through NHEJ of spontaneous DSBs, perhaps at stalled or blocked replication forks, perhaps by means of phosphorylation of RPA.