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




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Molecular Cancer

, 9:302

First Online: 23 November 2010Received: 15 June 2010Accepted: 23 November 2010

Abstract

BackgroundHuman 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.

ResultsIn 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.

ConclusionsIn 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.

List of abbreviationsE2FHTLV-I

PCNARb.

Electronic supplementary materialThe online version of this article doi:10.1186-1476-4598-9-302 contains supplementary material, which is available to authorized users.

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Autor: Hicham H Baydoun - Joanna Pancewicz - XueTao Bai - Christophe Nicot

Fuente: https://link.springer.com/







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