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    MECHANISMS OF MITOCHONDRIA-MEDIATED APOPTOSIS INDUCED BY CYTOTOXIC STRESS

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    Shelton_ku_0099D_10998_DATA_1.pdf (2.407Mb)
    Issue Date
    2010-06-04
    Author
    Shelton, Shary Nicole
    Publisher
    University of Kansas
    Format
    211 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
    Defects within the apoptotic pathway are thought to contribute to tumorigenesis and therapeutic resistance. Although most cytotoxic anti-cancer drugs are thought to activate the mitochondria-mediated apoptotic pathway, the precise mechanistic details remain unclear and, in some instances, controversial. We investigated the underlying molecular requirements necessary for mitochondria-mediated apoptosis induced by a DNA topoisomerase II inhibitor, a novel heat shock protein 90 (Hsp90) inhibitor, and elevated temperature in Jurkat T-lymphocytes. The data suggest that irreversible commitment to apoptosis induced by DNA-damage and heat-shock relies on a feed forward amplification loop of the initial death signal that is mediated by effector caspases and mitochondria. However, the pathway leading to cell death by inhibition of Hsp90 appeared to be in line with the traditional linear perspective of mitochondria-mediated apoptosis. Combined, the data suggest that different cytotoxic stressors use similar as well as distinct mechanisms to execute mitochondria-mediated apoptosis.
    URI
    http://hdl.handle.net/1808/6761
    Collections
    • Dissertations [4472]
    • Pharmacy Dissertations and Theses [118]

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    785-864-8983

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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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