Shared more. Cited more. Safe forever.
    • advanced search
    • submit works
    • about
    • help
    • contact us
    • login
    View Item 
    •   MOspace Home
    • University of Missouri-Columbia
    • Graduate School - MU Theses and Dissertations (MU)
    • Theses and Dissertations (MU)
    • Dissertations (MU)
    • 2008 Dissertations (MU)
    • 2008 MU dissertations - Freely available online
    • View Item
    •   MOspace Home
    • University of Missouri-Columbia
    • Graduate School - MU Theses and Dissertations (MU)
    • Theses and Dissertations (MU)
    • Dissertations (MU)
    • 2008 Dissertations (MU)
    • 2008 MU dissertations - Freely available online
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.
    advanced searchsubmit worksabouthelpcontact us

    Browse

    All of MOspaceCommunities & CollectionsDate IssuedAuthor/ContributorTitleIdentifierThesis DepartmentThesis AdvisorThesis SemesterThis CollectionDate IssuedAuthor/ContributorTitleIdentifierThesis DepartmentThesis AdvisorThesis Semester

    Statistics

    Most Popular ItemsStatistics by CountryMost Popular AuthorsStatistics by Referrer

    Alcohol induced histone acetylation mediated by histone acetyl transferase GCN5 in liver

    Choudhury, Mahua, 1977-
    View/Open
    [PDF] public.pdf (3.375Kb)
    [PDF] short.pdf (10.15Kb)
    [PDF] research.pdf (1.245Mb)
    Date
    2008
    Format
    Thesis
    Metadata
    [+] Show full item record
    Abstract
    Although 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.
    URI
    https://hdl.handle.net/10355/6866
    https://doi.org/10.32469/10355/6866
    Degree
    Ph. D.
    Thesis Department
    Physiology (Medicine) (MU)
    Rights
    OpenAccess.
    This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 License.
    Collections
    • 2008 MU dissertations - Freely available online
    • Medical Pharmacology and Physiology electronic theses and dissertations (MU)

    Send Feedback
    hosted by University of Missouri Library Systems
     

     


    Send Feedback
    hosted by University of Missouri Library Systems