ArticlePLoS pathogens2020
STING promotes NLRP3 localization in ER and facilitates NLRP3 deubiquitination to activate the inflammasome upon HSV-1 infection.
Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 papers, 3 of them syntheses that pooled it.
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Who cites it
156 citing papers in PubMed, 3 syntheses or guidelines pooled it, 224 citations in OpenAlex.
- The impact of post-translational modifications and subcellular localization on NLRP3 inflammasome activation: A systematic review.Cell communication and signaling : CCS · 2025Pooled it
- Association between herpesviruses and alzheimer's disease: a meta-analysis based on case-control studies.Molecular and cellular biochemistry · 2025Pooled it
- The cGAS-STING signaling pathway in the regulation of pulmonary infections: a systematic review.Frontiers in cellular and infection microbiology · 2025Pooled it
- Artificial platelets suppressing deep vein thrombosis via competitive adhesion.Bioactive materials · 2026Article
- The NLRP3 inflammasome at the crossroads of innate immune signaling and cell death.Cellular & molecular immunology · 2026Review
- Research progress on the mechanisms and animal models of Ménière's disease.Genes & diseases · 2026Review
- Regulatory NLRs in HSV-1 Infection: Direct Evidence, Comparative Mechanisms and Testable Hypotheses.Pathogens (Basel, Switzerland) · 2026Review
- DNA Sensing and Neuroinflammation: Mechanistic Insights into cGAS-STING Biology and Therapeutic Translation in Age-Related Neurodegenerative Diseases.Molecular neurobiology · 2026Review
- Neuroimmune Regulation of NLRP3 Signalling in Parkinson's Disease.Molecular neurobiology · 2026Review
- Review
- Emerging roles of the cGAS/STING pathway in cardiovascular diseases.The Journal of clinical investigation · 2026Review
- Mesoporous silica nanoparticle-mediated delivery of a synergistic 5-miRNA combination inhibits HSV-2 infection.Scientific reports · 2026Article
- STING is a key driver of Japanese encephalitis virus induced inflammatory response.Communications biology · 2026Article
- CerS6 orchestrates mitochondrial-immune crosstalk via BNIP3-dependent mitophagy suppression and mtDNA-STING/NLRP3 activation in acute lung injury.Cellular and molecular life sciences : CMLS · 2026Article
- The Role and Mechanism of the cGAS-STING/NLRP3 Signaling Axis-Regulated p38 MAPK/NF-κB Pathway in Manganese-Induced Tau Aggregation-Mediated Neurotoxicity.Environment & health (Washington, D.C.) · 2026Article
- NLR Inflammasomes in Viral Infections: From Molecular Mechanisms to Therapeutic Interventions.Viruses · 2026Review
- Mechanistic insights and therapeutic potential of targeting the cGAS-STING pathway in neurodegenerative diseases.Journal of neuroinflammation · 2026Review
- Pathophysiology and multi-target prevention strategies for cyclophosphamide-induced bladder injury.iScience · 2026Review
- STING agonists as antiviral agents.FEBS letters · 2026Review
- Molecular mechanisms of NLRP3 inflammasome activation.Experimental & molecular medicine · 2026Review
96 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
17 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
One of the fundamental reactions of the innate immune responses to pathogen infection is the release of pro-inflammatory cytokines, including IL-1β, processed by the NLRP3 inflammasome. The stimulator of interferon genes (STING) has the essential roles in innate immune response against pathogen infections. Here we reveal a distinct mechanism by which STING regulates the NLRP3 inflammasome activation, IL-1β secretion, and inflammatory responses in human cell lines, mice primary cells, and mice. Interestingly, upon HSV-1 infection and cytosolic DNA stimulation, STING binds to NLRP3 and promotes the inflammasome activation through two approaches. First, STING recruits NLRP3 and facilitates NLRP3 localization in the endoplasmic reticulum, thereby facilitating the inflammasome formation. Second, STING interacts with NLRP3 and attenuates K48- and K63-linked polyubiquitination of NLRP3, thereby promoting the inflammasome activation. Collectively, we demonstrate that the cGAS-STING-NLRP3 signaling is essential for host defense against HSV-1 infection.
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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.