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    The cell cycle and how it is steered by Kaposi's sarcoma-associated herpesvirus cyclin.

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    Authors
    Verschuren, Emmy W
    Jones, Nic
    Evan, Gerard I
    Affiliation
    Stanford University, Pathology Department, 300 Pasteur Drive, MC 5324, Stanford, CA 94305, USA.
    Issue Date
    2004-06
    
    Metadata
    Show full item record
    Abstract
    A timely coordination of cellular DNA synthesis and division cycles is governed by the temporal and spatial activation of cyclin-dependent kinases (Cdks). The primary regulation of Cdk activation is through binding to partner cyclin proteins. Several gammaherpesviruses encode a viral homologue of cellular cyclin D, which may function to deregulate host cell cycle progression. One of these is encoded by Kaposi's sarcoma-associated herpesvirus (KSHV) and is called K cyclin or viral cyclin (v-cyclin). v-Cyclin is expressed in most of the malignant cells that are associated with KSHV infection in humans, labelling v-cyclin as a putative viral oncogene. Here are described some of the major structural and functional properties of mammalian cyclin/Cdk complexes, some of which are phenocopied by v-cyclin. In addition, the molecular events leading to orderly progression through the G(1)/S and G/M cell cycle phases are reviewed. This molecular picture serves as a platform on which to explain v-cyclin-specific functional properties. Interesting but largely speculative issues concern the interplay between v-cyclin-mediated cell cycle deregulation and molecular progression of KSHV-associated neoplasms.
    Citation
    The cell cycle and how it is steered by Kaposi's sarcoma-associated herpesvirus cyclin. 2004, 85 (Pt 6):1347-61 J. Gen. Virol.
    Journal
    The Journal of General Virology
    URI
    http://hdl.handle.net/10541/78362
    PubMed ID
    15166416
    Type
    Article
    Language
    en
    ISSN
    0022-1317
    Collections
    All Paterson Institute for Cancer Research

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