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dc.contributor.authorVerschuren, Emmy W
dc.contributor.authorJones, Nic
dc.contributor.authorEvan, Gerard I
dc.date.accessioned2009-08-24T15:56:03Z
dc.date.available2009-08-24T15:56:03Z
dc.date.issued2004-06
dc.identifier.citationThe cell cycle and how it is steered by Kaposi's sarcoma-associated herpesvirus cyclin. 2004, 85 (Pt 6):1347-61 J. Gen. Virol.en
dc.identifier.issn0022-1317
dc.identifier.pmid15166416
dc.identifier.urihttp://hdl.handle.net/10541/78362
dc.description.abstractA 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.
dc.language.isoenen
dc.subject.meshAnimals
dc.subject.meshCatalytic Domain
dc.subject.meshCell Cycle
dc.subject.meshCell Cycle Proteins
dc.subject.meshCyclin-Dependent Kinases
dc.subject.meshCyclins
dc.subject.meshDNA-Binding Proteins
dc.subject.meshE2F Transcription Factors
dc.subject.meshEnzyme Activation
dc.subject.meshHerpesvirus 8, Human
dc.subject.meshHumans
dc.subject.meshMitosis
dc.subject.meshPhosphorylation
dc.subject.meshRetinoblastoma Protein
dc.subject.meshTranscription Factors
dc.subject.meshViral Proteins
dc.titleThe cell cycle and how it is steered by Kaposi's sarcoma-associated herpesvirus cyclin.en
dc.typeArticleen
dc.contributor.departmentStanford University, Pathology Department, 300 Pasteur Drive, MC 5324, Stanford, CA 94305, USA.en
dc.identifier.journalThe Journal of General Virologyen
html.description.abstractA 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.


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