ArticleScientific reports2017
PJA2 ubiquitinates the HIV-1 Tat protein with atypical chain linkages to activate viral transcription.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 28 citations in OpenAlex.
- USP45-mediated deubiquitination of HIV-1 Tat regulates viral transcription and latency.Frontiers in microbiology · 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 HIV-1 Transcriptional Program: From Initiation to Elongation Control.Journal of molecular biology · 2025Review
- Proximal protein landscapes of the type I interferon signaling cascade reveal negative regulation by PJA2.Nature communications · 2024Article
- Enhanced NF-κB activation via HIV-1 Tat-TRAF6 cross-talk.Science advances · 2024Article
- Ubiquitylation of BBSome is required for ciliary assembly and signaling.EMBO reports · 2023Article
- A modular CRISPR screen identifies individual and combination pathways contributing to HIV-1 latency.PLoS pathogens · 2023Article
- A siRNA screening of UBE2 family demonstrated that UBE2R1 had a high repressive effect on HIV Tat protein.Biochemistry and biophysics reports · 2022Article
- A functional map of HIV-host interactions in primary human T cells.Nature communications · 2022Article
- Interactome Analysis of Human Phospholipase D and Phosphatidic Acid-Associated Protein Network.Molecular & cellular proteomics : MCP · 2022Article
- Deubiquitinating Enzyme USP21 Inhibits HIV-1 Replication by Downregulating Tat Expression.Journal of virology · 2021Article
- HIV Nef-mediated Ubiquitination of BCL2: Implications in Autophagy and Apoptosis.Frontiers in immunology · 2021Article
- The ubiquitin-proteasome system is necessary for the replication of duck Tembusu virus.Microbial pathogenesis · 2019Article
- Role of the Ubiquitin Proteasome System (UPS) in the HIV-1 Life Cycle.International journal of molecular sciences · 2019Review
- Genetic variation and function of the HIV-1 Tat protein.Medical microbiology and immunology · 2019Review
- Pleiotropic roles of the ubiquitin-proteasome system during viral propagation.Life sciences · 2018Review
- Article
- SHMT2 and the BRCC36/BRISC deubiquitinase regulate HIV-1 Tat K63-ubiquitylation and destruction by autophagy.PLoS pathogens · 2018Article
- Post-translational Modification-Based Regulation of HIV Replication.Frontiers in microbiology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 2 countries.
Funding
Abstract
Transcription complexes that assemble at the HIV-1 promoter efficiently initiate transcription but generate paused RNA polymerase II downstream from the start site. The virally encoded Tat protein hijacks positive transcription elongation factor b (P-TEFb) to phosphorylate and activate this paused polymerase. In addition, Tat undergoes a series of reversible post-translational modifications that regulate distinct steps of the transcription cycle. To identify additional functionally important Tat cofactors, we performed RNAi knockdowns of sixteen previously identified Tat interactors and found that a novel E3 ligase, PJA2, ubiquitinates Tat in a non-degradative manner and specifically regulates the step of HIV transcription elongation. Interestingly, several different lysine residues in Tat can function as ubiquitin acceptor sites, and variable combinations of these lysines support both full transcriptional activity and viral replication. Further, the polyubiquitin chain conjugated to Tat by PJA2 can itself be assembled through variable ubiquitin lysine linkages. Importantly, proper ubiquitin chain assembly by PJA2 requires that Tat first binds its P-TEFb cofactor. These results highlight that both the Tat substrate and ubiquitin modification have plastic site usage, and this plasticity is likely another way in which the virus exploits the host molecular machinery to expand its limited genetic repertoire.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.