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    RETINOID-INDUCED APOPTOSIS AND PROLIFERATION OF HEPATOCYTES ARE MEDIATED BY DISTINCT NUCLEAR RECEPTORS

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    Bu_ku_0099D_10274_DATA_1.pdf (2.733Mb)
    Issue Date
    2009-04-07
    Author
    Bu, Pengli
    Publisher
    University of Kansas
    Format
    193 pages
    Type
    Dissertation
    Degree Level
    Ph.D.
    Discipline
    Pharmacology, Toxicology & Therapeutics
    Rights
    This item is protected by copyright and unless otherwise specified the copyright of this thesis/dissertation is held by the author.
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    Abstract
    Retinoids, derivatives of vitamin A, are important signaling molecules regulating cellular homeostasis including differentiation, apoptosis, and proliferation. In this dissertation, we examined the versatile effects of retinoids on human liver cell lines and mouse livers by genetic and biochemical approaches. The overall finding is that retinoids can cause opposing effects in liver cells. These effects are retinoid-specific, mediated by distinct nuclear receptors, and depend on intrinsic cellular settings. The first part of this dissertation studies the mechanism underlying the differential susceptibilities of human liver cancer cells to the apoptotic effect of a synthetic retinoid, fenretinide. The findings establish a role for the nuclear receptors RARβ; and Nur77 in mediating fenretinide effect. The second part of this dissertation investigates the mechanism responsible for 13-cis retinoic acid-induced liver cell proliferation. The results demonstrate that the activation of a signaling cascade PPARβ;/PDK-1/Akt is responsible for 13-cis retinoic acid-induced proliferation of liver cells.
    URI
    http://hdl.handle.net/1808/5385
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    • Dissertations [4473]
    • Pharmacy Dissertations and Theses [118]

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    785-864-8983

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    Lawrence, KS 66045
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    Contact KU ScholarWorks
    785-864-8983
    KU Libraries
    1425 Jayhawk Blvd
    Lawrence, KS 66045
    785-864-8983

    KU Libraries
    1425 Jayhawk Blvd
    Lawrence, KS 66045
    Image Credits
     

     

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