ArticleNature communications2025
TRIM23 mediates cGAS-induced autophagy in anti-HSV defense.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
11 citing papers in PubMed.
- Ubiquitin E3 ligase activity in TRIpartite Motif (TRIM) family proteins.Biochemical Society transactions · 2026Review
- Canonical and noncanonical autophagy in immunity.Immunity · 2026Review
- TRIM23 prevents adenovirus replication by p62-mediated selective autophagic degradation of viral E1A protein.PLoS pathogens · 2026Article
- Cell death network regulation in HSV infection: immune evasion versus host defense.Apoptosis : an international journal on programmed cell death · 2026Review
- Regulatory NLRs in HSV-1 Infection: Direct Evidence, Comparative Mechanisms and Testable Hypotheses.Pathogens (Basel, Switzerland) · 2026Review
- Resveratrol attenuates diabetic RGC degeneration through TRIM23-dependent VDAC1 ubiquitination and mitophagy.Cell communication and signaling : CCS · 2026Article
- Identification of extracellular vesicle microRNAs as potential facilitators of interferon-alpha escape in Marek's disease virus infection.Frontiers in cellular and infection microbiology · 2026Article
- Emerging Strategies for Antitumor Immunotherapy and Antiviral Defense Through the cGAS-STING Pathway.International journal of nanomedicine · 2026Review
- Deleterious variants in the autophagy-related gene RB1CC1/FIP200 impair immunity to SARS-CoV-2.Nature communications · 2025Article
- Mammalian innate antiviral defenses: beyond interferon.Journal of virology · 2025Review
- Caveolin-1 knockout improves CFA-induced inflammatory pain in adult mice through modulating the cGAS STING pathway and autophagy.PloS one · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
14 authors.
Funding
Abstract
The cGAS-STING pathway, well-known to elicit interferon (IFN) responses, is also a key inducer of autophagy upon virus infection or other stimuli. Whereas the mediators for cGAS-induced IFN responses are well characterized, much less is known about how cGAS elicits autophagy. Here, we report that TRIM23, a unique TRIM protein harboring both ubiquitin E3 ligase and GTPase activity, is crucial for cGAS-STING-dependent antiviral autophagy. Genetic ablation of TRIM23 impairs autophagic control of HSV-1 infection. HSV-1 infection or cGAS-STING stimulation induces TBK1-mediated TRIM23 phosphorylation at S39, which triggers TRIM23 autoubiquitination and GTPase activity and ultimately elicits autophagy. Fibroblasts from a patient with herpes simplex encephalitis heterozygous for a dominant-negative, kinase-inactivating TBK1 mutation fail to activate autophagy by TRIM23 and cGAS-STING. Our results thus identify the cGAS-STING-TBK1-TRIM23 axis as a key autophagy defense pathway and may stimulate new therapeutic interventions for viral or inflammatory diseases.
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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.