ArticleNucleic acids research2025
DDX6 interacts with DDX3X to repress translation in microRNA-mediated silencing.
Article in Nucleic acids research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- SAM68 is a multifunctional post-transcriptional regulator of cardiomyocyte differentiation.Nucleic acids research · 2026Article
- MicroRNAs in Heart Failure Pathogenesis and Progression: Mechanistic Control, Biomarker Potential, and Translational Perspectives.Life (Basel, Switzerland) · 2026Review
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Authors and funding
7 authors.
Funding
Abstract
DDX6 is known to repress messenger RNA (mRNA) translation and promote mRNA decay in microRNA-mediated silencing. In embryonic stem cells (ESCs), DDX6 primarily functions at the translation level, independent of mRNA destabilization; however, the precise molecular mechanism of how DDX6 represses translation remains unclear. Here, we identify DDX3X as a key downstream target of DDX6-mediated translational repression in ESCs. Conditional knockout of DDX3X demonstrates its essential role in microRNA (miRNA) silencing. Biochemical analyses reveal that DDX6 directly binds to DDX3X, with the C-terminal region of DDX6 being necessary for this interaction. ESCs lacking DDX6 and rescued with a DDX6 mutant that is defective in DDX3X interaction continue to exhibit miRNA silencing defects. Furthermore, the mutant DDX6 is unable to inhibit 48S preinitiation complex formation in vitro. These findings uncover a novel mechanism in which DDX6 represses target mRNA translation via its interaction with DDX3X.
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Registered trials
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