ArticleNature communications2019
Phosphorylation of MAVS/VISA by Nemo-like kinase (NLK) for degradation regulates the antiviral innate immune response.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 59 citations in OpenAlex.
- Review
- Sec8: a novel positive regulator of RIG-I in anti-RNA viral defense.Cell death & disease · 2026Article
- Old dogs-new tricks: multifaceted functions of MAVS beyond antivirus activity in human health and diseases.Cell & bioscience · 2025Review
- Unveiling EXOC4/SEC8: a key player in enhancing antiviral immunity by inhibiting the FBXL19-STING1-SQSTM1 signaling axis.Autophagy · 2025Article
- Atypical MAPKs in cancer.The FEBS journal · 2025Review
- PWWP3A disrupts the assembly of VISA/MAVS signalosome to inhibit innate immune response against RNA viruses.Nature communications · 2025Article
- Avian TRIM13 attenuates antiviral innate immunity by targeting MAVS for autophagic degradation.Autophagy · 2025Article
- Aggregatin is a mitochondrial regulator of MAVS activation to drive innate immunity.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Exploring the role of mitochondrial antiviral signaling protein in cardiac diseases.Frontiers in immunology · 2025Review
- PBLD enhances antiviral innate immunity by promoting the p53-USP4-MAVS signaling axis.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Evaluation of the diagnostic utility of immune microenvironment-related biomarkers in endometriosis using multidimensional transcriptomic data.Journal of assisted reproduction and genetics · 2024Article
- The Hemagglutinin of Influenza A Virus Induces Ferroptosis to Facilitate Viral Replication.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The deubiquitinase OTUD1 stabilizes NRF2 to alleviate hepatic ischemia/reperfusion injury.Redox biology · 2024Article
- MAVS Cys508 palmitoylation promotes its aggregation on the mitochondrial outer membrane and antiviral innate immunity.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- CLK2 mediates IκBα-independent early termination of NF-κB activation by inducing cytoplasmic redistribution and degradation.Nature communications · 2024Article
- Sex-specific circulating unconventional neutrophils determine immunological outcome of auto-inflammatory Behçet's uveitis.Cell discovery · 2024Article
- Dual modifying of MAVS at lysine 7 by SIRT3-catalyzed deacetylation and SIRT5-catalyzed desuccinylation orchestrates antiviral innate immunity.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Zebrafish TMEM47 is an effective blocker of IFN production during RNA and DNA virus infection.Journal of virology · 2023Article
- SAMHD1 impairs type I interferon induction through the MAVS, IKKε, and IRF7 signaling axis during viral infection.The Journal of biological chemistry · 2023Article
- Identification of SNPs Related toGenes · 2023Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MAVS is essential for antiviral immunity, but the molecular mechanisms responsible for its tight regulation remain poorly understood. Here, we show that NLK inhibits the antiviral immune response during viral infection by targeting MAVS for degradation. NLK depletion promotes virus-induced antiviral cytokine production and decreases viral replication, which is potently rescued by the reintroduction of NLK. Moreover, the depletion of NLK promotes antiviral effects and increases the survival times of mice after infection with VSV. NLK interacts with and phosphorylates MAVS at multiple sites on mitochondria or peroxisomes, thereby inducing the degradation of MAVS and subsequent inactivation of IRF3. Most importantly, a peptide derived from MAVS promotes viral-induced IFN-β production and antagonizes viral replication in vitro and in vivo. These findings provide direct insights into the molecular mechanisms by which phosphorylation of MAVS regulates its degradation and influences its activation and identify an important peptide target for propagating antiviral responses.
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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.