The cell cycle and how it is steered by Kaposi's sarcoma-associated herpesvirus cyclin Verschuren, Emmy W. and Jones, Nic and Evan, Gerard I.,, 85, 1347-1361 (2004), doi = https://doi.org/10.1099/vir.0.79812-0, publicationName = Microbiology Society, issn = 0022-1317, 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 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., language=, type=