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

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 inv...

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Main Authors: Kaori Asamitsu, Koh Fujinaga, Takashi Okamoto
Format: Article
Language:English
Published: MDPI AG 2018-04-01
Series:Molecules
Subjects:
Online Access:http://www.mdpi.com/1420-3049/23/4/933
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author Kaori Asamitsu
Koh Fujinaga
Takashi Okamoto
author_facet Kaori Asamitsu
Koh Fujinaga
Takashi Okamoto
author_sort Kaori Asamitsu
collection DOAJ
description 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.
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spelling doaj.art-9a94a12a186e41f28fee7af40698bd752022-12-22T01:27:13ZengMDPI AGMolecules1420-30492018-04-0123493310.3390/molecules23040933molecules23040933HIV Tat/P-TEFb Interaction: A Potential Target for Novel Anti-HIV TherapiesKaori Asamitsu0Koh Fujinaga1Takashi Okamoto2Department of Molecular and Cellular Biology, Nagoya City University Graduate School of Medical Sciences, Nagoya 467-8601, JapanDepartment of Medicine, Microbiology and Immunology, University of California, San Francisco, CA 94143-0703, USADepartment of Molecular and Cellular Biology, Nagoya City University Graduate School of Medical Sciences, Nagoya 467-8601, JapanTranscription 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.http://www.mdpi.com/1420-3049/23/4/933HIV transcriptionP-TEFbcyclin T1CDK9TatHEXIM1
spellingShingle Kaori Asamitsu
Koh Fujinaga
Takashi Okamoto
HIV Tat/P-TEFb Interaction: A Potential Target for Novel Anti-HIV Therapies
Molecules
HIV transcription
P-TEFb
cyclin T1
CDK9
Tat
HEXIM1
title HIV Tat/P-TEFb Interaction: A Potential Target for Novel Anti-HIV Therapies
title_full HIV Tat/P-TEFb Interaction: A Potential Target for Novel Anti-HIV Therapies
title_fullStr HIV Tat/P-TEFb Interaction: A Potential Target for Novel Anti-HIV Therapies
title_full_unstemmed HIV Tat/P-TEFb Interaction: A Potential Target for Novel Anti-HIV Therapies
title_short HIV Tat/P-TEFb Interaction: A Potential Target for Novel Anti-HIV Therapies
title_sort hiv tat p tefb interaction a potential target for novel anti hiv therapies
topic HIV transcription
P-TEFb
cyclin T1
CDK9
Tat
HEXIM1
url http://www.mdpi.com/1420-3049/23/4/933
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AT kohfujinaga hivtatptefbinteractionapotentialtargetfornovelantihivtherapies
AT takashiokamoto hivtatptefbinteractionapotentialtargetfornovelantihivtherapies