ArticleCell reports2018
Inhibition of Microprocessor Function during the Activation of the Type I Interferon Response.
Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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.
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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.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Article
- Characterization of RNA interference in the cnidarian Nematostella vectensis reveals partial target silencing but lack of small RNA amplification.PLoS biology · 2026Article
- DGCR8 haploinsufficiency leads to primate-specific RNA dysregulation and pluripotency defects.Nucleic acids research · 2025Article
- DGCR8 deficiency impairs macrophage growth and unleashes the interferon response to mycobacteria.Life science alliance · 2021Article
- Determination of primary microRNA processing in clinical samples by targeted pri-miR-sequencing.RNA (New York, N.Y.) · 2020Article
- The RNA binding protein Quaking represses host interferon response by downregulating MAVS.RNA biology · 2020Article
- ILF3 contributes to the establishment of the antiviral type I interferon program.Nucleic acids research · 2020Article
- Extracellular RNA in viral-host interactions: Thinking outside the cell.Wiley interdisciplinary reviews. RNA · 2019Review
- Article
- Crosstalk Between Mammalian Antiviral Pathways.Non-coding RNA · 2019Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Type I interferons (IFNs) are central components of the antiviral response. Most cell types respond to viral infections by secreting IFNs, but the mechanisms that regulate correct expression of these cytokines are not completely understood. Here, we show that activation of the type I IFN response regulates the expression of miRNAs in a post-transcriptional manner. Activation of IFN expression alters the binding of the Microprocessor complex to pri-miRNAs, reducing its processing rate and thus leading to decreased levels of a subset of mature miRNAs in an IRF3-dependent manner. The rescue of Microprocessor function during the antiviral response downregulates the levels of IFN-β and IFN-stimulated genes. All these findings support a model by which the inhibition of Microprocessor activity is an essential step to induce a robust type I IFN response in mammalian cells.
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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.