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 Blood, 15 January 2006, Vol. 107, No. 2, pp. 725-732.
Prepublished online as a Blood First Edition Paper on September 13, 2005; DOI 10.1182/blood-2005-06-2534.

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NEOPLASIA

KSHV viral cyclin inactivates p27KIP1 through Ser10 and Thr187 phosphorylation in proliferating primary effusion lymphomas

Grzegorz Sarek, Annika Järviluoma, and Päivi M. Ojala

From the Molecular Cancer Biology Program, Institute of Biomedicine, Biomedicum Helsinki, Finland.

Kaposi sarcoma herpesvirus (KSHV) infection is consistently associated with primary effusion lymphomas (PELs) that are non-Hodgkin lymphomas of B-cell origin. All PEL cells are latently infected with KSHV and express latent viral proteins such as the viral cyclin (v-cyclin), which has previously been implicated in down-regulation of cell-cycle inhibitor p27KIP1 levels via phosphorylation on Thr187. PEL cells retain high levels of p27KIP1 but yet proliferate actively, which has left the biologic significance of this p27KIP1 destabilization somewhat elusive. We have recently demonstrated that v-cyclin and p27KIP1 stably associate in PEL cells. Here we demonstrate that v-cyclin together with its kinase partner CDK6 phosphorylates the associated p27KIP1 in PEL cells, which represent a biologically relevant model system for KSHV pathobiology. During latent viral replication p27KIP1 was phosphorylated by v-cyclin-CDK6 predominantly on Ser10, which enhances its cytoplasmic localization. Interestingly, upon reactivation of KSHV lytic cycle, v-cyclin-CDK6 phosphorylated p27KIP1 on Thr187, which resulted in down-regulation of p27KIP1 protein levels. These findings indicate that v-cyclin modulates the cell-cycle inhibitory function of p27KIP1 by phosphorylation in PELs, and also suggest a novel role for v-cyclin in the lytic reactivation of KSHV. (Blood. 2006;107:725-732)


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