H
Hilary A. Coller
Researcher at University of California, Los Angeles
Publications - 103
Citations - 28264
Hilary A. Coller is an academic researcher from University of California, Los Angeles. The author has contributed to research in topics: Cell cycle & Cellular differentiation. The author has an hindex of 40, co-authored 95 publications receiving 25863 citations. Previous affiliations of Hilary A. Coller include Rutgers University & University of California.
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Journal ArticleDOI
Staying alive: metabolic adaptations to quiescence.
James R. Valcourt,Johanna M.S. Lemons,Erin M. Haley,Mina L Kojima,Olukunle O. Demuren,Hilary A. Coller +5 more
TL;DR: This review compares and contrast the metabolic changes that occur with quiescence in different model systems, including Saccharomyces cerevisiae, mammalian lymphocytes and hematopoietic stem cells, and the PI3Kinase/TOR signaling pathway.
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Lactate dehydrogenase activity drives hair follicle stem cell activation
Aimee Flores,John C. Schell,Abigail S. Krall,David Jelinek,Matilde Miranda,Melina Grigorian,Daniel Braas,Andrew C. White,Jessica L. Zhou,Nicholas A. Graham,Nicholas A. Graham,Thomas G. Graeber,Pankaj Seth,Denis Evseenko,Hilary A. Coller,Jared Rutter,Jared Rutter,Heather R. Christofk,William E. Lowry +18 more
TL;DR: It is demonstrated that HFSCs utilize glycolytic metabolism and produce significantly more lactate than other cells in the epidermis, and small molecules that increase lactate production by stimulating Myc levels or inhibiting Mpc1 carrier activity and can topically induce the hair cycle are identified.
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Mitochondrial mutational spectra in human cells and tissues
Konstantin Khrapko,Hilary A. Coller,Paulo C. André,Xiao Cheng Li,John S. Hanekamp,William G. Thilly +5 more
TL;DR: The similarity of the hotspot sets in vivo and in vitro leads us to conclude that human mitochondrial point mutations in the sequence studied are primarily spontaneous in origin and arise either from DNA replication error or reactions of DNA with endogenous metabolites.
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Cell-by-cell scanning of whole mitochondrial genomes in aged human heart reveals a significant fraction of myocytes with clonally expanded deletions
Konstantin Khrapko,Konstantin Khrapko,Natalya Bodyak,Natalya Bodyak,William G. Thilly,Nathalie J. Van Orsouw,Xiaomin Zhang,Hilary A. Coller,Thomas T. Perls,Melissa P. Upton,Jan Vijg,Jeanne Y. Wei +11 more
TL;DR: Analysis of more than 350 individual cells that were derived from three middle-aged and four centenarian donors demonstrates that while most of the cells contain no deletions, in certain cardiomyocytes a significant portion of the mtDNA molecules carried one particular deletion.
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Is cancer a metabolic disease
TL;DR: This article reviews recent research in the field of cancer metabolism, raising the following questions: Why do cancer cells shift their metabolism in this way?