ArticleEMBO reports2022
Interferon-mediated repression of miR-324-5p potentiates necroptosis to facilitate antiviral defense.
Article in EMBO reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Single-cell RNA-seq combined with bulk RNA-seq analysis identifies necroptosis-related genes as therapeutic targets for periodontitis.BMC medical genomics · 2025Article
- Luciferase Reporter Systems in Investigating Interferon Antiviral Innate Immunity.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Mechanistic Insights into Influenza A Virus-Induced Cell Death and Emerging Treatment Strategies.Veterinary sciences · 2024Review
- Research progress on miRNAs function in the interaction between human infectious viruses and hosts: A review.Biomolecules & biomedicine · 2024Review
- Bisphenol A Regulates the TNFR1 Pathway and Excessive ROS Mediated by miR-26a-5p/ADAM17 Axis to Aggravate Selenium Deficiency-Induced Necroptosis in Broiler Veins.Biological trace element research · 2024Article
- IE1 of Human Cytomegalovirus Inhibits Necroptotic Cell Death via Direct and Indirect Modulation of the Necrosome Complex.Viruses · 2024Article
- Integrated analysis of miRNA-mRNA expression of newly emerging swine H3N2 influenza virus cross-species infection with tree shrews.Virology journal · 2024Article
- The dance of macrophage death: the interplay between the inevitable and the microenvironment.Frontiers in immunology · 2024Review
- Article
- The double-edged functions of necroptosis.Cell death & disease · 2023Review
- Interferon-mediated repression of miR-324-5p potentiates necroptosis to facilitate antiviral defense.EMBO reports · 2022Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mixed lineage kinase domain-like protein (MLKL) is the terminal effector of necroptosis, a form of regulated necrosis. Optimal activation of necroptosis, which eliminates infected cells, is critical for antiviral host defense. MicroRNAs (miRNAs) regulate the expression of genes involved in various biological and pathological processes. However, the roles of miRNAs in necroptosis-associated host defense remain largely unknown. We screened a library of miRNAs and identified miR-324-5p as the most effective suppressor of necroptosis. MiR-324-5p downregulates human MLKL expression by specifically targeting the 3'UTR in a seed region-independent manner. In response to interferons (IFNs), miR-324-5p is downregulated via the JAK/STAT signaling pathway, which removes the posttranscriptional suppression of MLKL mRNA and facilitates the activation of necroptosis. In influenza A virus (IAV)-infected human primary macrophages, IFNs are induced, leading to the downregulation of miR-324-5p. MiR-324-5p overexpression attenuates IAV-associated necroptosis and enhances viral replication, whereas deletion of miR-324-5p potentiates necroptosis and suppresses viral replication. Hence, miR-324-5p negatively regulates necroptosis by manipulating MLKL expression, and its downregulation by IFNs orchestrates optimal activation of necroptosis in host antiviral defense.
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