ArticleJournal of virology2010
DDX6 (Rck/p54) is required for efficient hepatitis C virus replication but not for internal ribosome entry site-directed translation.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 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
72 citing papers in PubMed, 107 citations in OpenAlex.
- At the crossroads of immunity and hijacking: dual roles of DDX proteins during host-virus interactions.Frontiers in cellular and infection microbiology · 2026Review
- Review
- DDX RNA helicases: key players in cellular homeostasis and innate antiviral immunity.Journal of virology · 2024Review
- RNA sequestration in P-bodies sustains myeloid leukaemia.Nature cell biology · 2024Article
- Review
- RNA Helicase DDX6 Regulates A-to-I Editing and Neuronal Differentiation in Human Cells.International journal of molecular sciences · 2023Article
- miR-193b-3p Promotes Proliferation of Goat Skeletal Muscle Satellite Cells through Activating IGF2BP1.International journal of molecular sciences · 2022Article
- Human coronaviruses disassemble processing bodies.PLoS pathogens · 2022Article
- Host Cellular RNA Helicases Regulate SARS-CoV-2 Infection.Journal of virology · 2022Article
- Eukaryotic mRNA Decapping Activation.Frontiers in genetics · 2022Review
- Enterovirus 71 2A Protease Inhibits P-Body Formation To Promote Viral RNA Synthesis.Journal of virology · 2021Article
- Effect of P-body component Mov10 on HCV virus production and infectivity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- The RNA Helicase DDX6 Controls Cellular Plasticity by Modulating P-Body Homeostasis.Cell stem cell · 2019Article
- Strategies for Success. Viral Infections and Membraneless Organelles.Frontiers in cellular and infection microbiology · 2019Review
- RNA decay is an antiviral defense in plants that is counteracted by viral RNA silencing suppressors.PLoS pathogens · 2018Article
- Eukaryotic translation initiation factor 4AII contributes to microRNA-122 regulation of hepatitis C virus replication.Nucleic acids research · 2018Article
- The Interplay between the RNA Decay and Translation Machinery in Eukaryotes.Cold Spring Harbor perspectives in biology · 2018Review
- The Multiples Fates of the Flavivirus RNA Genome During Pathogenesis.Frontiers in genetics · 2018Review
- Signals Involved in Regulation of Hepatitis C Virus RNA Genome Translation and Replication.Frontiers in microbiology · 2018Review
- DDX6 Represses Aberrant Activation of Interferon-Stimulated Genes.Cell reports · 2017Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
DDX6 (Rck/p54) is an evolutionarily conserved member of the SF2 DEAD-box RNA helicase family that contributes to the regulation of translation and storage and the degradation of cellular mRNAs. It interacts with multiple proteins and is a component of the micro-RNA (miRNA)-induced silencing complex (miRISC). Since miRNA-122 (miR-122) is essential for efficient hepatitis C virus (HCV) replication, we investigated the requirement for DDX6 in HCV replication in cultured hepatoma cells. Small interfering RNA (siRNA)-mediated knockdown of DDX6 and rescue with an siRNA-resistant mutant demonstrated that DDX6 expression is indeed required for optimal HCV replication. However, DDX6 knockdown did not impair miR-122 biogenesis or alter HCV responsiveness to miR-122 supplementation. Overexpression of DDX6 fused to EYFP (EYFP-DDX6) enhanced replication, whereas a helicase-deficient mutant with a substitution in the conserved DEAD-box motif II (DQAD) had a dominant-negative effect, reducing HCV yields. Coimmunoprecipitation experiments revealed an intracellular complex containing DDX6, HCV core protein, and both viral and cellular RNAs, the formation of which was dependent upon the C-terminal domain of DDX6 but not DDX6 helicase activity. However, since DDX6 abundance influenced the replication of subgenomic HCV RNAs lacking core sequence, the relevance of this complex is uncertain. Importantly, DDX6 knockdown caused minimal reductions in cellular proliferation, generally stimulated cellular translation ([(35)S]Met incorporation), and did not impair translation directed by the HCV internal ribosome entry site. Thus, DDX6 helicase activity is essential for efficient HCV replication, reflecting essential roles for DDX6 in HCV genome amplification and/or maintenance of cellular homeostasis.
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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.