ArticleJournal of molecular biology2018
DDX17 Specifically, and Independently of DDX5, Controls Use of the HIV A4/5 Splice Acceptor Cluster and Is Essential for Efficient Replication of HIV.
Article in Journal of molecular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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
12 citing papers in PubMed, 22 citations in OpenAlex.
- Tools for Experimental and Computational Genome-Wide Analysis of the Function of DDX5 and DDX17 Helicases in RNA Processing.Methods in molecular biology (Clifton, N.J.) · 2027Article
- DDX17 and viral infection.Virulence · 2026Review
- RNA helicases, DDX5 and DDX17, facilitate lytic reactivation of gammaherpesviruses.PLoS pathogens · 2025Article
- PAK4 promotes the cytoskeletal organization and meiotic maturation via phosphorylating DDX17 in oocyte.Cell communication and signaling : CCS · 2025Article
- Review
- DDX RNA helicases: key players in cellular homeostasis and innate antiviral immunity.Journal of virology · 2024Review
- DDX5: an expectable treater for viral infection- a literature review.Annals of translational medicine · 2022Review
- DEAD-ly Affairs: The Roles of DEAD-Box Proteins on HIV-1 Viral RNA Metabolism.Frontiers in cell and developmental biology · 2022Review
- Article
- Intragenic recruitment of NF-κB drives splicing modifications upon activation by the oncogene Tax of HTLV-1.Nature communications · 2020Article
- DDX5 potentiates HIV-1 transcription as a co-factor of Tat.Retrovirology · 2020Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
HIV splicing involves five splice donor and eight splice acceptor sequences which, together with cryptic splice sites, generate over 100 mRNA species. Ninety percent of both partially spliced and fully spliced transcripts utilize the intrinsically weak A4/A5 3' splice site cluster. We show that DDX17, but not its close paralog DDX5, specifically controls the usage of this splice acceptor group. In its absence, production of the viral envelope protein and other regulatory and accessory proteins is grossly reduced, while Vif, which uses the A1 splice acceptor, is unaffected. This is associated with a profound decrease in viral export from the cell. Loss of Vpu expression causing upregulation of cellular Tetherin compounds the phenotype. DDX17 utilizes distinct RNA binding motifs for its role in efficient HIV replication, and we identify RNA binding motifs essential for its role, while the Walker A, Walker B (DEAD), Q motif and the glycine doublet motif are all dispensable. We show that DDX17 interacts with SRSF1/SF2 and the heterodimeric auxiliary factor U2AF65/35, which are essential splicing factors in the generation of Rev and Env/Vpu transcripts.
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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.