ArticlePLoS pathogens2023
TRIM21 restricts influenza A virus replication by ubiquitination-dependent degradation of M1.
Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 30 citations in OpenAlex.
- TRIM21 blocks DDX3X-driven stress granule formation during Mycobacterium tuberculosis infection via a non-canonical E3 ligase mechanism.PLoS pathogens · 2026Article
- Adaptive mutations at lysine residues of PRRSV-2 nsp12 enable evasion of host proteasomal degradation to promote subgenomic RNA synthesis.Journal of virology · 2026Article
- ZFP91 restricts RSV replication by driving K48-linked ubiquitination and proteasomal degradation of M2-1.Cellular and molecular life sciences : CMLS · 2026Article
- TRIM7 Inhibits Rabies Virus Replication by Promoting K48-Linked Ubiquitination and Degradation of RABV-M.Emerging microbes & infections · 2026Article
- TRIM13 Positively Regulates the NF-κB Signaling Pathway Induced by Encephalomyocarditis Virus.Viruses · 2026Article
- Duck plague virus LORF2 utilizes RNF34 to inhibit antiviral innate immunity by ubiquitination and degradation of IRF7.PLoS pathogens · 2026Article
- Post-translational modification networks as master regulators of influenza virus replication, host adaptation, and immune evasion.Frontiers in immunology · 2026Review
- Differential host responses by the type I and III interferons in primary differentiated human nasal epithelial cells are a determinant of antiviral activity.Frontiers in pharmacology · 2026Article
- The roles of post-translational modifications in the pathogenesis of RNA viruses: allies or adversaries?Frontiers in microbiology · 2026Review
- TRIM29 inhibits PRRSV replication by targeting nsp11 for degradation.Journal of virology · 2025Article
- Enhanced replication of a contemporary avian influenza A H9N2 virus in human respiratory organoids.Emerging microbes & infections · 2025Article
- Ribosomal protein L35 negatively regulates FMDV replication by recruiting AMFR to promote the ubiquitination and degradation of VP2.Journal of virology · 2025Article
- Differential Host Responses and Viral Replication of Highly Pathogenic Avian Influenza H5N1 Strains in Diverse Cell Lines with a Raw Milk Supplement.Life (Basel, Switzerland) · 2025Article
- Heat shock protein A1L restricts influenza A virus by ubiquitination of NA.Journal of virology · 2025Article
- TRIM31 triggers colorectal carcinogenesis and progression by maintaining YBX1 protein stability through ubiquitination modification.Cell death & disease · 2025Article
- Clade 2.3.4.4b highly pathogenic avian influenza H5N1 viruses: knowns, unknowns, and challenges.Journal of virology · 2025Review
- MARCH8 promotes the proteasomal degradation of foot-and-mouth disease virus VP1, VP2, and VP3 to negatively regulate viral replication.Veterinary research · 2025Article
- Preparedness, prevention and control related to zoonotic avian influenza.EFSA journal. European Food Safety Authority · 2025Article
- Retinol binding protein 4 restricts PCV2 replication via selective autophagy degradation of viral ORF1 protein.Communications biology · 2024Article
- TRIM35 triggers cardiac remodeling by regulating SLC7A5-mediated amino acid transport and mTORC1 activation in fibroblasts.Cell communication and signaling : CCS · 2024Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tripartite motif-containing protein 21 (TRIM21), an E3 ubiquitin ligase, plays a critical role in the host antiviral response. However, the mechanism and antiviral spectrum of TRIM21 in influenza A virus (IAV) remain unclear. Here, we report that TRIM21 inhibits the replication of various IAV subtypes by targeting matrix protein 1 (M1) from H3/H5/H9, but not H1 and H7 M1. Mechanistically, TRIM21 binds to the residue R95 of M1 and facilitates K48 ubiquitination of M1 K242 for proteasome-dependent degradation, leading to the inhibition of H3, H5, and H9 IAV replication. Interestingly, the recombinant viruses with M1 R95K or K242R mutations were resistance to TRIM21 and exhibited more robust replication and severe pathogenicity. Moreover, the amino acid sequence M1 proteins, mainly from avian influenza such as H5N1, H7N9, H9N2, ranging from 1918 to 2022, reveals a gradual dominant accumulation of the TRIM21-driven R95K mutation when the virus jumps into mammals. Thus, TRIM21 in mammals' functions as a host restriction factor and drives a host adaptive mutation of influenza A virus.
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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 Socratic graph.