[-] Show simple item record

dc.contributor.advisorShukla, Shivendra D.en_US
dc.contributor.authorChoudhury, Mahua, 1977-en_US
dc.date.issued2008eng
dc.date.submitted2008 Summeren_US
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.en_US
dc.descriptionTitle from PDF of title page (University of Missouri--Columbia, viewed on April 6, 2010).en_US
dc.descriptionIncludes bibliographical referencesen_US
dc.descriptionVita.en_US
dc.descriptionThesis advisor: Shivendra D. Shukla.en_US
dc.description"August 2008"en_US
dc.descriptionPh. D. University of Missouri-Columbia 2008.en_US
dc.descriptionDissertations, Academic -- University of Missouri--Columbia -- physiology (Medicine).en_US
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.en_US
dc.format.extentxv, 181 pagesen_US
dc.identifier.oclc603557930en_US
dc.identifier.otherChoudhuryM-110509-D11715en_US
dc.identifier.urihttp://hdl.handle.net/10355/6866
dc.publisherUniversity of Missouri--Columbiaen_US
dc.relation.ispartof2008 Freely available dissertations (MU)en_US
dc.relation.ispartofcommunityUniversity of Missouri-Columbia. Graduate School. Theses and Dissertations. Dissertations. 2008 Dissertations
dc.subject.lcshAlcoholic liver diseasesen_US
dc.subject.lcshHistones -- Metabolismen_US
dc.subject.lcshHistones -- Effect of drugs onen_US
dc.subject.lcshAcetyltransferasesen_US
dc.subject.lcshAlcohols -- Receptors -- Effect of drugs onen_US
dc.subject.lcshHistone deacetylase -- Metabolismen_US
dc.subject.meshLiver Diseases, Alcoholic -- etiologyen_US
dc.subject.meshHistones -- metabolismen_US
dc.subject.meshHistones -- drug effectsen_US
dc.subject.meshHistone Acetyltransferasesen_US
dc.subject.meshAlcohols -- pharmacologyen_US
dc.subject.meshHistone Deacetylases -- metabolismen_US
dc.titleAlcohol induced histone acetylation mediated by histone acetyl transferase GCN5 in liveren_US
dc.typeThesisen_US
thesis.degree.disciplinePhysiology (Medicine)en_US
thesis.degree.disciplinePhysiology (Medicine)eng
thesis.degree.grantorUniversity of Missouri--Columbiaen_US
thesis.degree.levelDoctoralen_US
thesis.degree.namePh. D.en_US


Files in this item

[PDF]
[PDF]
[PDF]

This item appears in the following Collection(s)

[-] Show simple item record