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Jonathan Coffman

Researcher at University of Tennessee Health Science Center

Publications -  14
Citations -  866

Jonathan Coffman is an academic researcher from University of Tennessee Health Science Center. The author has contributed to research in topics: Gene & Gene expression. The author has an hindex of 9, co-authored 14 publications receiving 806 citations. Previous affiliations of Jonathan Coffman include Saba University School of Medicine & Barry University.

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Cellular Localization of Huntingtin in Striatal and Cortical Neurons in Rats: Lack of Correlation with Neuronal Vulnerability in Huntington’s Disease

TL;DR: The finding that huntingtin is not consistently found in striatal projection neurons but is abundant instriatal cholinergic interneurons (which survive in Huntington’s disease) suggests that the mutation in huntingtin that causes HD may not directly kill neurons.
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Gat1p, a GATA Family Protein Whose Production Is Sensitive to Nitrogen Catabolite Repression, Participates in Transcriptional Activation of Nitrogen-Catabolic Genes in Saccharomyces cerevisiae

TL;DR: It is demonstrated that another positive regulator, designated Gat1p, participates in the transcription of NCR-sensitive genes and is able to weakly activate transcription when tethered upstream of a reporter gene devoid of upstream activation sequence elements.
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Cross regulation of four GATA factors that control nitrogen catabolic gene expression in Saccharomyces cerevisiae.

TL;DR: It is shown that a fourth member of the yeast GATA family, the Dal80p homolog Deh1p, also negatively regulates expression of some, but not all, nitrogen catabolic genes, i.e., GAP1, DAL80, and UGA4 expression increases in a deh1 delta mutant.
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Understanding the Impact of Omega-3 Rich Diet on the Gut Microbiota

TL;DR: Some of the health-related benefits of omega-3 may be due, in part, to increases in butyrate-producing bacteria, which may shed light on the mechanisms explaining the effects of Omega-3 in several chronic diseases and may also serve as an existing foundation for tailoring personalized medical treatments.
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Saccharomyces cerevisiae GATA sequences function as TATA elements during nitrogen catabolite repression and when Gln3p is excluded from the nucleus by overproduction of Ure2p.

TL;DR: The data suggest that the mechanism underlying NCR involves the cytoplasmic association of Ure2p with Gln 3p, an interaction that prevents Gln3p from reaching it is binding sites upstream of NCR-sensitive genes.