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dc.contributor.authorBaydoun, Hicham H
dc.contributor.authorPancewicz, Joanna
dc.contributor.authorBai, XueTao
dc.contributor.authorNicot, Christophe
dc.date.accessioned2011-01-07T17:15:58Z
dc.date.available2011-01-07T17:15:58Z
dc.date.issued2010-11-23en_US
dc.identifier.urihttp://hdl.handle.net/2271/912en_US
dc.description.abstractAbstract Background Human T-cell leukemia virus type I (HTLV-I) has efficiently adapted to its host and establishes a persistent infection characterized by low levels of viral gene expression and slow proliferation of HTLV-I infected cells over decades. We have previously found that HTLV-I p30 is a negative regulator of virus expression. Results In this study we show that p30 targets multiple cell cycle checkpoints resulting in a delayed entry into S phase. We found that p30 binds to cyclin E and CDK2 and prevents the formation of active cyclin E-CDK2 complexes. In turn, this decreases the phosphorylation levels of Rb and prevents the release of E2F and its transcriptional activation of genes required for G1/S transition. Our studies also show that HTLV-II p28 does not bind cyclin E and does not affect cell cycle progression. Conclusions In contrast to HTLV-I, the HTLV-II-related retrovirus is not oncogenic in humans. Here we report that the HTLV-I p30 delays cell cycle progression while its homologue, HTLV-II p28, does not, providing evidence for important differences between these two related retrovirus proteins.
dc.titleHTLV-I p30 inhibits multiple S phase entry checkpoints, decreases cyclin E-CDK2 interactions and delays cell cycle progression.
dc.typeArticleen_US
dc.identifier.doi10.1186/1476-4598-9-302en_US
dc.date.updated2010-12-09T16:02:21Z
dc.description.versionPeer Reviewed
dc.rights.holderBaydoun et al.; licensee BioMed Central Ltd.
dc.rights.accessrightsopenAccessen_US


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