Cyclin T1 stabilizes expression levels of HIV-1 Tat in cells
dc.contributor.author | Imai, Kenichi | en_US |
dc.contributor.author | Asamitsu, Kaori | en_US |
dc.contributor.author | Victoriano, Ann florence B. | en_US |
dc.contributor.author | Cueno, Marni E. | en_US |
dc.contributor.author | Fujinaga, Koh | en_US |
dc.contributor.author | Okamoto, Takashi | en_US |
dc.date.accessioned | 2011-01-13T19:38:18Z | |
dc.date.available | 2011-01-13T19:38:18Z | |
dc.date.issued | 2009-12 | en_US |
dc.identifier.citation | Imai, Kenichi; Asamitsu, Kaori; Victoriano, Ann florence B.; Cueno, Marni E.; Fujinaga, Koh; Okamoto, Takashi; (2009). "Cyclin T1 stabilizes expression levels of HIV-1 Tat in cells." FEBS Journal 276(23): 7124-7133. <http://hdl.handle.net/2027.42/78606> | en_US |
dc.identifier.issn | 1742-464X | en_US |
dc.identifier.issn | 1742-4658 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/78606 | |
dc.description.abstract | Transcription from HIV-1 proviral DNA is a rate-determining step for HIV-1 replication. Interaction between the cyclin T1 (CycT1) subunit of positive transcription elongation factor b (P-TEFb) and the Tat transactivator protein of HIV-1 is crucial for viral transcription. CycT1 also interacts directly with the transactivation-responsive element (TAR) located on the 5′end of viral mRNA, as well as with Tat through the Tat–TAR recognition motif (TRM). These molecular interactions represent a critical step for stimulation of HIV transcription. Thus, Tat and CycT1 are considered to be feasible targets for the development of novel anti-HIV therapies. In this study, we demonstrate that CycT1 is positively involved in the Tat protein stability. Selective degradation of CycT1 by small interfering RNA (siRNA) culminated in proteasome-mediated degradation of Tat and eventual inhibition of HIV-1 gene expression. We noted that the siRNA-mediated knockdown of CycT1 could inhibit HIV-1 transcription without affecting cell viability and Tat mRNA levels. These findings clearly indicate that CycT1 is a feasible therapeutic target, and inactivation or depletion of CycT1 should effectively inhibit HIV replication by destabilizing Tat and suppressing Tat-mediated HIV transcription. | en_US |
dc.format.extent | 407214 bytes | |
dc.format.extent | 3106 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.publisher | Blackwell Publishing Ltd | en_US |
dc.subject.other | Cyclin T1 | en_US |
dc.subject.other | HIV | en_US |
dc.subject.other | Protein Stability | en_US |
dc.subject.other | Tat | en_US |
dc.subject.other | Transcription | en_US |
dc.title | Cyclin T1 stabilizes expression levels of HIV-1 Tat in cells | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Biological Chemistry | en_US |
dc.subject.hlbtoplevel | Science | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Biological Chemistry, University of Michigan Medical School, Ann Arbor, MI, USA | en_US |
dc.contributor.affiliationother | Department of Molecular and Cellular Biology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan | en_US |
dc.identifier.pmid | 20064163 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/78606/1/j.1742-4658.2009.07424.x.pdf | |
dc.identifier.doi | 10.1111/j.1742-4658.2009.07424.x | en_US |
dc.identifier.source | FEBS Journal | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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