ArticleProceedings of the National Academy of Sciences of the United States of America2016
Mint3 potentiates TLR3/4- and RIG-I-induced IFN-β expression and antiviral immune responses.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- Aromatic microbial metabolite hippuric acid enhances inflammatory responses in macrophages via TLR-MyD88 signaling and lipid remodeling.Cell reports · 2026Article
- Toll-like receptors in innate immunity and inflammation: from fundamental biology to clinic insights.Immunity & inflammation · 2026Review
- Macrophage ATG16L1 expression suppresses metabolic dysfunction-associated steatohepatitis progression by promoting lipophagy.Clinical and molecular hepatology · 2024Article
- Article
- Mint3 as a Potential Target for Cooling Down HIF-1α-Mediated Inflammation and Cancer Aggressiveness.Biomedicines · 2023Review
- CILP, a Putative Gene Associated With Immune Infiltration in Breast Cancer Brain Metastases.Frontiers in genetics · 2022Article
- Mint3 depletion-mediated glycolytic and oxidative alterations promote pyroptosis and prevent the spread of Listeria monocytogenes infection in macrophages.Cell death & disease · 2021Article
- Targeting Pin1 for Modulation of Cell Motility and Cancer Therapy.Biomedicines · 2021Review
- Hypothermic oxygenated perfusion inhibits HECTD3-mediated TRAF3 polyubiquitination to alleviate DCD liver ischemia-reperfusion injury.Cell death & disease · 2021Article
- Mint3 is dispensable for pancreatic and kidney functions in mice.Biochemistry and biophysics reports · 2020Article
- UAF1 deubiquitinase complexes facilitate NLRP3 inflammasome activation by promoting NLRP3 expression.Nature communications · 2020Article
- Redox homeostasis maintained by GPX4 facilitates STING activation.Nature immunology · 2020Article
- KAT8 selectively inhibits antiviral immunity by acetylating IRF3.The Journal of experimental medicine · 2019Article
- HECTD3 mediates TRAF3 polyubiquitination and type I interferon induction during bacterial infection.The Journal of clinical investigation · 2018Article
- Prolyl isomerase Pin1: a promoter of cancer and a target for therapy.Cell death & disease · 2018Review
- MiR-22 sustains NLRP3 expression and attenuates H. pylori-induced gastric carcinogenesis.Oncogene · 2018Article
- Viruses Seen by Our Cells: The Role of Viral RNA Sensors.Journal of immunology research · 2018Review
- USP1-UAF1 deubiquitinase complex stabilizes TBK1 and enhances antiviral responses.The Journal of experimental medicine · 2017Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type I IFNs (IFN-α/β) play crucial roles in the elimination of invading viruses. Multiple immune cells including macrophages recognize viral infection through a variety of pattern recognition receptors, such as Toll-like receptors (TLRs) and retinoic acid-inducible gene-I (RIG-I)-like receptors, and initiate type I IFN secretion and subsequent antiviral immune responses. However, the mechanisms by which host immune cells can produce adequate amounts of type I IFNs and then eliminate viruses effectively remain to be further elucidated. In the present study, we show that munc18-1-interacting protein 3 (Mint3) expression can be markedly induced during viral infection in macrophages. Mint3 enhances TLR3/4- and RIG-I-induced IRF3 activation and IFN-β production by promoting K63-linked polyubiquitination of TNF receptor-associated factor 3 (TRAF3). Consistently, Mint3 deficiency greatly attenuated antiviral immune responses and increased viral replication. Therefore, we have identified Mint3 as a physiological positive regulator of TLR3/4 and RIG-I-induced IFN-β production and have outlined a feedback mechanism for the control of antiviral immune 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.