ArticleThe EMBO journal2024
The helicase domain of human Dicer prevents RNAi-independent activation of antiviral and inflammatory pathways.
Article in The EMBO journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Tuning intracellular immunity by Nodamura virus B2 protein enhances self-amplifying RNA activity.Nature communications · 2026Article
- Canonical microRNA loss drives tumor development, implicating therapeutic efficacy of enoxacin in angiosarcoma.RNA (New York, N.Y.) · 2026Article
- Exogenous dsRNA made accessible to Dicer by two eukaryotic RNA-dependent RNA polymerases in Paramecium tetraurelia.Communications biology · 2026Article
- Bat Dicer antiviral role and subcellular localization differ upon alphavirus infection in two distinct species.PLoS pathogens · 2025Article
- Cross-cohort integrative multi-omics analysis of cancer essential gene ATP6V0B to dissect functional characteristics and clinical implications in breast cancer.World journal of surgical oncology · 2025Article
- Dicer is cleaved by the Leader protease encoded by foot-and-mouth disease virus to promote infection in mammalian cells.Science advances · 2025Article
- In vivo Dicer-2 interactome during viral infection reveals novel pro and antiviral factors in Drosophila melanogaster.PLoS pathogens · 2025Article
- Enhanced RNAi does not provide efficient innate antiviral immunity in mice.Nucleic acids research · 2025Article
- The human Dicer helicase domain is capable of ATP hydrolysis and single-stranded nucleic acid binding.BMC biology · 2024Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
In mammalian somatic cells, the relative contribution of RNAi and the type I interferon response during viral infection is unclear. The apparent inefficiency of antiviral RNAi might be due to self-limiting properties and mitigating co-factors of the key enzyme Dicer. In particular, the helicase domain of human Dicer appears to be an important restriction factor of its activity. Here, we study the involvement of several helicase-truncated mutants of human Dicer in the antiviral response. All deletion mutants display a PKR-dependent antiviral phenotype against certain viruses, and one of them, Dicer N1, acts in a completely RNAi-independent manner. Transcriptomic analyses show that many genes from the interferon and inflammatory response pathways are upregulated in Dicer N1 expressing cells. We show that some of these genes are controlled by NF-kB and that blocking this pathway abrogates the antiviral phenotype of Dicer N1. Our findings highlight the crosstalk between Dicer, PKR, and the NF-kB pathway, and suggest that human Dicer may have repurposed its helicase domain to prevent basal activation of antiviral and inflammatory pathways.
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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.