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dc.contributor.advisorShukla, Shivendra D.eng
dc.contributor.authorChoudhury, Mahua, 1977-eng
dc.date.issued2008eng
dc.date.submitted2008 Summereng
dc.descriptionThe entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file.eng
dc.descriptionTitle from PDF of title page (University of Missouri--Columbia, viewed on April 6, 2010).eng
dc.descriptionIncludes bibliographical referenceseng
dc.descriptionVita.eng
dc.descriptionThesis advisor: Shivendra D. Shukla.eng
dc.description"August 2008"eng
dc.descriptionPh. D. University of Missouri-Columbia 2008.eng
dc.descriptionDissertations, Academic -- University of Missouri--Columbia -- physiology (Medicine).eng
dc.description.abstractAlthough several mechanisms have identified for alcoholic liver disease, at present there are no precise mechanisms for liver injury. We have observed that surrogate alcohols increases histone H3 acetylation selectively at Lys 9 (H3AcK9) via metabolites in primary rat hepatocytes. Alcohols and metabolites both increased the HAT activity. However, propionate and butyrate also decreased HDAC activity. In addition, oxidative stress also mediates ethanol induced histone acetylation and ADH1 gene expression. It is likely that both NADPH oxidase and mitochondria derived ROS are involved. The study presented here also identifies for the first time the specific HAT, GCN5, responsible for ethanol induced H3AcK9 in human hepatoma cell overexpressing ADH1 (VA-13). siRNA knock down of GCN5 decreased both ethanol induced H3AcK9 and HAT activity. In summery, we conclude that ethanol increases H3AcK9 via modulation of GCN5 in the liver. These original findings may contribute to a better understanding of the mechanism underlying the pathogenesis of alcoholic liver disease.eng
dc.format.extentxv, 181 pageseng
dc.identifier.oclc603557930eng
dc.identifier.otherChoudhuryM-110509-D11715eng
dc.identifier.urihttp://hdl.handle.net/10355/6866eng
dc.publisherUniversity of Missouri--Columbiaeng
dc.relation.ispartof2008 Freely available dissertations (MU)eng
dc.relation.ispartofcommunityUniversity of Missouri-Columbia. Graduate School. Theses and Dissertations. Dissertations. 2008 Dissertationseng
dc.subject.lcshAlcoholic liver diseaseseng
dc.subject.lcshHistones -- Metabolismeng
dc.subject.lcshHistones -- Effect of drugs oneng
dc.subject.lcshAcetyltransferaseseng
dc.subject.lcshAlcohols -- Receptors -- Effect of drugs oneng
dc.subject.lcshHistone deacetylase -- Metabolismeng
dc.subject.meshLiver Diseases, Alcoholic -- etiologyeng
dc.subject.meshHistones -- metabolismeng
dc.subject.meshHistones -- drug effectseng
dc.subject.meshHistone Acetyltransferaseseng
dc.subject.meshAlcohols -- pharmacologyeng
dc.subject.meshHistone Deacetylases -- metabolismeng
dc.titleAlcohol induced histone acetylation mediated by histone acetyl transferase GCN5 in livereng
dc.typeThesiseng
thesis.degree.disciplinePhysiology (Medicine) (MU)eng
thesis.degree.grantorUniversity of Missouri--Columbiaeng
thesis.degree.levelDoctoraleng
thesis.degree.namePh. D.eng


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