ArticleCellular & molecular immunology2014
Suppression of innate antiviral response by severe acute respiratory syndrome coronavirus M protein is mediated through the first transmembrane domain.
Article in Cellular & molecular immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed, 111 citations in OpenAlex.
- Viral Mechanisms and Drug Influences on Janus Kinase/Signal Transducers and Activators of Transcription (JAK/STAT) Pathway in Human Coronaviruses Infection: A Systematic Review.Health science reports · 2026Review
- PEDV Structural Proteins with Emphasis on M Protein as an Immunomodulatory Factor in Porcine Innate Immunity.Life (Basel, Switzerland) · 2025Review
- A Comprehensive View on the Mechanisms of Coronavirus Escaping Innate Immunity.Veterinary sciences · 2025Review
- Anti-interferon armamentarium of human coronaviruses.Cellular and molecular life sciences : CMLS · 2025Review
- A20 as a Potential Therapeutic Target for COVID-19.Immunity, inflammation and disease · 2025Review
- Structural proteins of human coronaviruses: what makes them different?Frontiers in cellular and infection microbiology · 2024Review
- Exploring type I interferon pathway: virulent vs. attenuated strain of African swine fever virus revealing a novel function carried by MGF505-4R.Frontiers in immunology · 2024Article
- Molecular mechanisms of human coronavirus NL63 infection and replication.Virus research · 2023Review
- Is there an association between peri-diagnostic vaccination and clinical outcomes in COVID-19 patients?Antimicrobial stewardship & healthcare epidemiology : ASHE · 2023Article
- Structure and dynamics of membrane protein in SARS-CoV-2.Journal of biomolecular structure & dynamics · 2022Article
- Immunogenic and reactogenic efficacy of Covaxin and Covishield: a comparative review.Immunologic research · 2022Review
- Mechanisms of Antiviral Immune Evasion of SARS-CoV-2.Journal of molecular biology · 2022Review
- A Review of the Potential Effects of Melatonin in Compromised Mitochondrial Redox Activities in Elderly Patients With COVID-19.Frontiers in nutrition · 2022Review
- COVID-19: Immunology, Immunopathogenesis and Potential Therapies.International reviews of immunology · 2022Review
- Evolution and Epidemiology of SARS-CoV-2 Virus.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Comparing the Nucleocapsid Proteins of Human Coronaviruses: Structure, Immunoregulation, Vaccine, and Targeted Drug.Frontiers in molecular biosciences · 2022Review
- The Robustness of Cellular Immunity Determines the Fate of SARS-CoV-2 Infection.Frontiers in immunology · 2022Review
- SARS-CoV-2 spike protein induces inflammation via TLR2-dependent activation of the NF-κB pathway.eLife · 2021Article
- Immunopathology and Immunopathogenesis of COVID-19, what we know and what we should learn.Gene reports · 2021Review
- Molecular Insights into the Crosstalk Between Immune Inflammation Nexus and SARS-CoV-2 Virus.Current microbiology · 2021Review
19 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Coronaviruses have developed various measures to evade innate immunity. We have previously shown that severe acute respiratory syndrome (SARS) coronavirus M protein suppresses type I interferon (IFN) production by impeding the formation of functional TRAF3-containing complex. In this study, we demonstrate that the IFN-antagonizing activity is specific to SARS coronavirus M protein and is mediated through its first transmembrane domain (TM1) located at the N terminus. M protein from human coronavirus HKU1 does not inhibit IFN production. Whereas N-linked glycosylation of SARS coronavirus M protein has no influence on IFN antagonism, TM1 is indispensable for the suppression of IFN production. TM1 targets SARS coronavirus M protein and heterologous proteins to the Golgi apparatus, yet Golgi localization is required but not sufficient for IFN antagonism. Mechanistically, TM1 is capable of binding with RIG-I, TRAF3, TBK1 and IKKε, and preventing the interaction of TRAF3 with its downstream effectors. Our work defines the molecular architecture of SARS coronavirus M protein required for suppression of innate antiviral response.
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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.