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Blood, 15 November 2004, Vol. 104, No. 10, pp. 3349-3354. Prepublished online as a Blood First Edition Paper on July 22, 2004; DOI 10.1182/blood-2004-05-1798. This Article Full Text (PDF) All Versions of this Article: 2004-05-1798v1 104/10/3349    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Jarviluoma, A. Articles by Ojala, P. M Search for Related Content PubMed PubMed Citation Articles by Jarviluoma, A. Articles by Ojala, P. M Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted May 11, 2004 Accepted July 5, 2004 KSHV viral cyclin binds to p27KIP1 in primary effusion lymphomas Annika Jarviluoma, Sonja Koopal, Susanna Rasanen, Tomi P Makela, and Paivi M Ojala* Molecular Cancer Biology Program, Biomedicum Helsinki & Haartman Institute, University of Helsinki, Helsinki, Finland Molecular Cancer Biology Program, Biomedicum Helsinki & Haartman Institute, University of Helsinki, Helsinki, Finland; Institute of Biomedicine, and Helsinki University Central Hospital, Biomedicum Helsinki, University of Helsinki, Finland * Corresponding author; email: Paivi.Ojala{at}helsinki.fi. Primary effusion lymphomas (PELs) represent a unique non-Hodgkin's lymphoma, which is consistently infected by Kaposi's sarcoma herpesvirus (KSHV). PEL cells express high levels of the cell cycle inhibitor p27KIP1 and yet proliferate actively. KSHV genome encodes a viral cyclin homolog, v-cyclin, which has previously been implicated in downregulation of p27KIP1 levels. To address how PEL cells can tolerate high p27KIP1 we investigated functional interactions between v-cyclin and p27KIP1 using PEL derived cell lines as a model system. Here we demonstrate that v-cyclin and p27KIP1 stably associate in PEL cells in vivo suggesting an attractive model by which p27KIP1 is inactivated in the actively proliferating PEL cells. Moreover, we show that v-cyclin and CDK6 form an active kinase without p27KIP1 and that CDK6 is the in vivo catalytic subunit of v-cyclin in PEL cells. These findings suggest that KSHV may promote oncogenesis in PEL by expressing v-cyclin which both overrides negative cell cycle controls present in the PEL precursor cells and induces a strong proliferative signal via CDK6 kinase activity. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. Jarviluoma, E. S. Child, G. Sarek, P. Sirimongkolkasem, G. Peters, P. M. Ojala, and D. J. Mann Phosphorylation of the Cyclin-Dependent Kinase Inhibitor p21Cip1 on Serine 130 Is Essential for Viral Cyclin-Mediated Bypass of a p21Cip1-Imposed G1 Arrest. Mol. Cell. Biol., March 1, 2006; 26(6): 2430 - 2440. [Abstract] [Full Text] [PDF] G. Sarek, A. Jarviluoma, and P. M. Ojala KSHV viral cyclin inactivates p27KIP1 through Ser10 and Thr187 phosphorylation in proliferating primary effusion lymphomas Blood, January 15, 2006; 107(2): 725 - 732. [Abstract] [Full Text] [PDF]

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