HTLV-I p30 inhibits multiple S phase entry checkpoints, decreases cyclin E-CDK2 interactions and delays cell cycle progression.

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dc.contributor.author Baydoun, Hicham H
dc.contributor.author Pancewicz, Joanna
dc.contributor.author Bai, XueTao
dc.contributor.author Nicot, Christophe
dc.date.accessioned 2011-01-07T17:15:58Z
dc.date.available 2011-01-07T17:15:58Z
dc.date.issued 2010-11-23
dc.identifier http://dx.doi.org/10.1186/1476-4598-9-302
dc.identifier.uri http://hdl.handle.net/2271/912
dc.description.abstract Abstract 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.title HTLV-I p30 inhibits multiple S phase entry checkpoints, decreases cyclin E-CDK2 interactions and delays cell cycle progression.
dc.type Journal Article
dc.date.updated 2010-12-09T16:02:21Z
dc.description.version Peer Reviewed
dc.language.rfc3066 en
dc.rights.holder Baydoun et al.; licensee BioMed Central Ltd.

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