C
Caroline C. Philpott
Researcher at National Institutes of Health
Publications - 79
Citations - 5884
Caroline C. Philpott is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Ferritin & Saccharomyces cerevisiae. The author has an hindex of 41, co-authored 75 publications receiving 5027 citations.
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Journal ArticleDOI
A Cytosolic Iron Chaperone That Delivers Iron to Ferritin
TL;DR: Human poly (rC)–binding protein 1 (PCBP1) increased the amount of iron loaded into ferritin when expressed in yeast and can function as a cytosolic iron chaperone in the delivery of iron to ferrit in vitro.
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Iron uptake in fungi: a system for every source.
TL;DR: Fungi have a remarkable capacity to take up iron when present in any of a wide variety of forms, which include free iron ions, low-affinity iron chelates, siderophore-iron chelate, transferrin, heme, and hemoglobin, and some of which are present in plants and animals, as well.
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Regulation of Cation Balance in Saccharomyces cerevisiae
TL;DR: This review summarizes the current understanding of how cation balance is achieved and modulated in baker’s yeast and discusses the mechanisms that allow cells to maintain appropriate intracellular cation concentrations when challenged by extreme conditions, i.e., either limited availability or toxic levels in the environment.
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Response to Iron Deprivation in Saccharomyces cerevisiae
TL;DR: Iron is an essential nutrient for almost every organism because iron cofactors, such as heme and iron-sulfur clusters (ISC), are required for the activity of numerous cellular enzymes involved in a wide range of cellular processes.
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Transcriptional remodeling in response to iron deprivation in Saccharomyces cerevisiae.
Minoo Shakoury-Elizeh,John Tiedeman,Jared Rashford,Tracey Ferea,Janos Demeter,Emily Garcia,Ronda J. Rolfes,Patrick O. Brown,David Botstein,Caroline C. Philpott +9 more
TL;DR: Evidence is provided that yeast subjected to iron deprivation undergo a transcriptional remodeling, resulting in a shift from iron-dependent to parallel, but iron-independent, metabolic pathways.