ArticleCell & bioscience2014
Modulation of the stability and activities of HIV-1 Tat by its ubiquitination and carboxyl-terminal region.
Article in Cell & bioscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- TRIP12 promotes HIV-1 replication and latency reactivation by stabilizing Tat via USP7-mediated deubiquitination.Journal of virology · 2026Article
- YAP Inhibits HIV-1 transcription and promotes HIV-1 latency by regulating E3 ubiquitin ligase UHRF1 mediated tat degradation.PLoS pathogens · 2026Article
- FBXO45 restricts HIV-1 replication by inducing SQSTM1/p62-mediated autophagic degradation of Tat.Journal of virology · 2025Article
- The Involvement of Ubiquitination and SUMOylation in Retroviruses Infection and Latency.Viruses · 2023Review
- Review
- Article
- Review
- Deubiquitinating Enzyme USP21 Inhibits HIV-1 Replication by Downregulating Tat Expression.Journal of virology · 2021Article
- Alteration of cell junctions during viral infection.Thoracic cancer · 2020Review
- Presence of Tat and transactivation response element in spinal fluid despite antiretroviral therapy.AIDS (London, England) · 2019Article
- The host cell ubiquitin ligase protein CHIP is a potent suppressor of HIV-1 replication.The Journal of biological chemistry · 2019Article
- Proteasomal Degradation Machinery: Favorite Target of HIV-1 Proteins.Frontiers in microbiology · 2018Review
- Post-translational Modification-Based Regulation of HIV Replication.Frontiers in microbiology · 2018Review
- Review
- Immune regulator ABIN1 suppresses HIV-1 transcription by negatively regulating the ubiquitination of Tat.Retrovirology · 2017Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe transactivator of transcription (Tat) protein of human immunodeficiency virus type 1 (HIV-1) is known to undergo ubiquitination. However, the roles of ubiquitination in regulating Tat stability and activities are unclear. In addition, although the 72- and 86-residue forms are commonly used for in vitro studies, the 101-residue form is predominant in the clinical isolates of HIV-1. The influence of the carboxyl-terminal region of Tat on its functions remains unclear.
resultsIn this study, we find that Tat undergoes lysine 48-linked ubiquitination and is targeted to proteasome-dependent degradation. Expression of various ubiquitin mutants modulates Tat activities, including the transactivation of transcription, induction of apoptosis, interaction with tubulin, and stabilization of microtubules. Moreover, the 72-, 86- and 101-residue forms of Tat also exhibit different stability and aforementioned activities.
conclusionsOur findings demonstrate that the ubiquitination and carboxyl-terminal region of Tat are critical determinants of its stability and activities.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.