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Molecules 2018, 23(4), 933;

HIV Tat/P-TEFb Interaction: A Potential Target for Novel Anti-HIV Therapies

Department of Molecular and Cellular Biology, Nagoya City University Graduate School of Medical Sciences, Nagoya 467-8601, Japan
Department of Medicine, Microbiology and Immunology, University of California, San Francisco, CA 94143-0703, USA
Authors to whom correspondence should be addressed.
Academic Editor: Takaomi Sanda
Received: 30 March 2018 / Revised: 13 April 2018 / Accepted: 14 April 2018 / Published: 17 April 2018
(This article belongs to the Special Issue Transcription Factors as Therapeutic Targets)
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Transcription is a crucial step in the life cycle of the human immunodeficiency virus type 1 (HIV 1) and is primarily involved in the maintenance of viral latency. Both viral and cellular transcription factors, including transcriptional activators, suppressor proteins and epigenetic factors, are involved in HIV transcription from the proviral DNA integrated within the host cell genome. Among them, the virus-encoded transcriptional activator Tat is the master regulator of HIV transcription. Interestingly, unlike other known transcriptional activators, Tat primarily activates transcriptional elongation and initiation by interacting with the cellular positive transcriptional elongation factor b (P-TEFb). In this review, we describe the molecular mechanism underlying how Tat activates viral transcription through interaction with P-TEFb. We propose a novel therapeutic strategy against HIV replication through blocking Tat action. View Full-Text
Keywords: HIV transcription; P-TEFb; cyclin T1; CDK9; Tat; HEXIM1 HIV transcription; P-TEFb; cyclin T1; CDK9; Tat; HEXIM1

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Asamitsu, K.; Fujinaga, K.; Okamoto, T. HIV Tat/P-TEFb Interaction: A Potential Target for Novel Anti-HIV Therapies. Molecules 2018, 23, 933.

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