ArticleScientific reports2016
TRIM14 inhibits hepatitis C virus infection by SPRY domain-dependent targeted degradation of the viral NS5A protein.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 90 citations in OpenAlex.
- Identification ofFrontiers in immunology · 2018Trial
- Innovative Strategies for the Targeted Degradation of Viral Proteins: Paving the Way for Next-Generation Therapeutics.Pharmaceutics · 2025Review
- TRIM14 restricts tembusu virus infection through degrading viral NS1 protein and activating type I interferon signaling.PLoS pathogens · 2025Article
- Identification of TRIM21 and TRIM14 as Antiviral Factors Against Langat and Zika Viruses.Viruses · 2025Article
- Redirecting E3 ubiquitin ligases for targeted protein degradation with heterologous recognition domains.The Journal of biological chemistry · 2025Article
- Regulation of viral replication by host restriction factors.Frontiers in immunology · 2025Review
- Emerging discoveries on the role of TRIM14: from diseases to immune regulation.Cell death discovery · 2024Review
- The Role of Tripartite Motif Family Proteins in Chronic Liver Diseases: Molecular Mechanisms and Therapeutic Potential.Biomolecules · 2024Review
- Emerging roles of tripartite motif family proteins (TRIMs) in breast cancer.Cancer medicine · 2024Review
- An Antiviral Role for TRIM14 in Ebola Virus Infection.The Journal of infectious diseases · 2023Article
- JMJD2D stabilises and cooperates with HBx protein to promote HBV transcription and replication.JHEP reports : innovation in hepatology · 2023Article
- Tripartite motif‑containing 14 may aggravate cardiac hypertrophy via the AKT signalling pathway in neonatal rat cardiomyocytes and transgenic mice.Molecular medicine reports · 2023Article
- Expression Profiling of the Tripartite Motif Family Genes in Chronic Hepatitis C Patients.ACS omega · 2023Article
- PcTrim prevents early infection with white spot syndrome virus by inhibiting AP1-induced endocytosis.Cell communication and signaling : CCS · 2023Article
- Rabies virus uniquely reprograms the transcriptome of human monocyte-derived macrophages.Frontiers in cellular and infection microbiology · 2023Article
- TRIM proteins in hepatocellular carcinoma.Journal of biomedical science · 2022Review
- TRIM22 suppresses Zika virus replication by targeting NS1 and NS3 for proteasomal degradation.Cell & bioscience · 2022Article
- LncRNA GAS6-AS1 facilitates tumorigenesis and metastasis of colorectal cancer by regulating TRIM14 through miR-370-3p/miR-1296-5p and FUS.Journal of translational medicine · 2022Article
- Mapping of molecular interactions between human E3 ligase TRIM69 and Dengue virus NS3 protease using hydrogen-deuterium exchange mass spectrometry.Cellular and molecular life sciences : CMLS · 2022Article
- Dual-Role Ubiquitination Regulation Shuttling the Entire Life Cycle of the Flaviviridae.Frontiers in microbiology · 2022Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tripartite motif 14 (TRIM14) was reported to function as a mitochondrial signaling adaptor in mediating innate immune responses. However, the involvement of TRIM14 in host defense against viral infection and molecular mechanisms remain unclear. Here, we demonstrated that enforced expression of TRIM14 could potently inhibit the infection and replication of HCV in hepatocytes, whereas TRIM14 knockout cells became more susceptible to HCV infection. Interestingly, further experiments revealed that such anti-HCV activity was independent of activating the NF-κB or interferon pathways but required the C-terminal SPRY domain of no signaling capacity. In searching for mechanisms how TRIM14 exerts its antiviral function we found that TRIM14 interacted with HCV encoded non-structural protein NS5A and could strongly induce its degradation dependent on the NS5A1 subdomain. Interestingly extensive domain mapping analyses revealed that NS5A degradation was mediated by the highly conserved SPRY domain of TRIM14, which might involve the K48 ubiquitination pathway. Collectively, our work uncovered a new mechanism responsible for host defense against HCV infection, and could potentially aid the development of novel anti-HCV therapeutics.
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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.