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

¹ Stanford University, Pathology Department, 300 Pasteur Drive, MC 5324, Stanford, CA 94305, USA
² Paterson Institute for Cancer Research, Christie Hospital NHS Trust, Manchester M20 4BX, UK
³ Cancer Research Institute and Department of Cellular and Molecular Pharmacology, University of California San Francisco, CA 94143-0875, USA

Correspondence
Gerard I. Evan
GEvan{at}cc.ucsf.edu

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 G₁/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.

Published online ahead of print on 19 March 2004 as DOI 10.1099/vir.0.79812-0.

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