ArticleCell death & disease2017
ARRDC4 regulates enterovirus 71-induced innate immune response by promoting K63 polyubiquitination of MDA5 through TRIM65.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 48 citations in OpenAlex.
- Sensing of double-stranded RNA in human cells: molecular mechanisms and cellular consequences.Biochemical Society transactions · 2026Review
- Structural and functional perspectives on DEAD-box RNA helicases in the rubber tree cold stress response.Frontiers in plant science · 2026Review
- ARRDC1 inhibits the replication of Semliki Forest virus by regulating the ubiquitination and degradation of viral nsP4.Journal of virology · 2025Article
- ARRDC4-mediated glycolysis enhances innate immunity to influenza A virus through fructose-1,6-bisphosphate.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- ARRDC3 promotes lysosome-mediated YAP degradation to inhibit enterovirus replication.Virologica Sinica · 2025Article
- Article
- Direct RNA sequencing reveals chicken post-transcriptional modifications in response to Campylobacter jejuni inoculation.BMC genomics · 2025Article
- The Magic and Mystery of TRIM65 in Diseases.Current medicinal chemistry · 2025Review
- TRIM65 promotes renal cell carcinoma through ubiquitination and degradation of BTG3.Cell death & disease · 2024Article
- Identification of HDAC9 and ARRDC4 as potential biomarkers and targets for treatment of type 2 diabetes.Scientific reports · 2024Article
- Role of protein Post-translational modifications in enterovirus infection.Frontiers in microbiology · 2024Review
- SARS-CoV-2 Nsp8 suppresses MDA5 antiviral immune responses by impairing TRIM4-mediated K63-linked polyubiquitination.PLoS pathogens · 2023Article
- LPS inhibits TRIM65 expression in macrophages and C57BL/6J mouse by activating the ERK1/2 signaling pathway.Experimental and therapeutic medicine · 2023Article
- TRAF3 activates STING-mediated suppression of EV-A71 and target of viral evasion.Signal transduction and targeted therapy · 2023Article
- Thioredoxin-Interacting Protein in Cancer and Diabetes.Antioxidants & redox signaling · 2022Review
- α-Arrestins and Their Functions: From Yeast to Human Health.International journal of molecular sciences · 2022Review
- The genomic signatures of natural selection in admixed human populations.American journal of human genetics · 2022Article
- Transcriptome analysis provides new insights into cold adaptation of corsac fox (Ecology and evolution · 2022Article
- IKKε isoform switching governs the immune response against EV71 infection.Communications biology · 2021Article
- Regulation of RIG-I-like receptor-mediated signaling: interaction between host and viral factors.Cellular & molecular immunology · 2021Review
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Enterovirus 71 (EV71) is the main causative agent of hand, foot and mouth disease (HFMD), which induces significantly elevated levels of cytokines and chemokines, leading to local or system inflammation and severe complications, whereas the underlying regulatory mechanisms and the inflammatory pathogenesis remain elusive. ARRDC4 is one member of arrestins family, having important roles in glucose metabolism and G-protein-coupled receptors (GPCRs) related physiological and pathological processes, however, the function of ARRDC4 in innate immune system is largely unknown. Here we identified that ARRDC4 expression was increased after EV71 infection in THP-1-derived macrophages and verified in EV71-infected HFMD patients and the healthy candidates. The expression level of ARRDC4 was positively correlated with the serum concentration of IL-6, TNF-α and CCL3 in clinical specimens. ARRDC4 interacted with MDA5 via the arrestin-like N domain, and further recruited TRIM65 to enhance the K63 ubiquitination of MDA5, resulting in activation of the downstream innate signaling pathway and transcription of proinflammatory cytokines during EV71 infection. Our data highlight new function of ARRDC4 in innate immunity, contributing to the better understanding about regulation of MDA5 activation after EV71 infection, and also suggest ARRDC4 may serve as a potential target for intervention of EV71-induced inflammatory response.
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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.