ArticleThe Journal of experimental medicine2017
Protein kinase D at the Golgi controls NLRP3 inflammasome activation.
Article in The Journal of experimental medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 184 papers, 3 of them syntheses that pooled it.
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Who cites it
184 citing papers in PubMed, 3 syntheses or guidelines pooled it, 280 citations in OpenAlex.
- The NLRP3 inflammasome in osteoarthritis: a systematic review of traditional, complementary, and integrative medicine efficacy and underlying mechanisms.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026Pooled it
- The impact of post-translational modifications and subcellular localization on NLRP3 inflammasome activation: A systematic review.Cell communication and signaling : CCS · 2025Pooled it
- MAM kinases: physiological roles, related diseases, and therapeutic perspectives-a systematic review.Cellular & molecular biology letters · 2025Pooled it
- AMBRA1 allosterically activates NLRP3 by releasing its autoinhibition.Nature immunology · 2026Article
- Post-translational modifications in Neuroimmune cells during neuroinflammation: integrated regulatory networks and therapeutic opportunities.Biology direct · 2026Review
- A Review on Structural Insights into NLRP3 and NEK7: Domain Architecture, Subcellular Localization, and Their Interaction in Inflammasome Assembly and Signaling.Molecular neurobiology · 2026Review
- Neuroimmune Regulation of NLRP3 Signalling in Parkinson's Disease.Molecular neurobiology · 2026Review
- Spatial control of NLRP3 inflammasome assembly by membrane lipid composition.Communications biology · 2026Review
- The Mechanism of NLRP3 Inflammasome Activation and Its Roles in Chronic Rhinosinusitis.World journal of otorhinolaryngology - head and neck surgery · 2026Review
- Non-decameric NLRP3 reveals a TGN/MTOC-distal pathway of inflammasome activation.Nature communications · 2026Article
- Durumamide A Inhibits NLRP3 Assembly, Limiting Pro-Inflammatory Signaling in Human Gingival Fibroblasts.Journal of periodontal research · 2026Article
- The role of mitochondria-associated membranes in tumorigenesis.Discover oncology · 2026Review
- Molecular mechanisms of NLRP3 inflammasome activation.Experimental & molecular medicine · 2026Review
- Diverse Scaffolds Facilitate NLRP3 Clustering and Inflammasome Formation in Response to Perturbations in Cell Homeostasis.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- The NLRP3 Inflammasome: Mechanisms of Activation, Regulation, and Therapeutic Opportunities.MedComm · 2026Review
- Post-translational modifications of NLRP3: to prime or not to prime?Trends in immunology · 2026Review
- Mitochondrial Dysfunction in Acute Kidney Injury: Intersections Between Chemotherapy and Novel Cancer Immunotherapies.Biomolecules · 2026Review
- Hypoxia-conditioned BMSC exosomes improve short-term spinal cord injury outcomes via the miR-615-3p/PDE4C-mediated cAMP/PKA pathway.Stem cell research & therapy · 2026Article
- 14-3-3ε-dependent deubiquitination and translocation of NLRP3 activates the inflammasome during sepsis.JCI insight · 2026Article
- Organelle stress in NLRP3 inflammasome: a central mediator of neurodegenerative diseases.Molecular neurodegeneration · 2026Review
124 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
19 authors at 6 institutions in 3 countries.
Funding
Abstract
The inflammasomes are multiprotein complexes sensing tissue damage and infectious agents to initiate innate immune responses. Different inflammasomes containing distinct sensor molecules exist. The NLRP3 inflammasome is unique as it detects a variety of danger signals. It has been reported that NLRP3 is recruited to mitochondria-associated endoplasmic reticulum membranes (MAMs) and is activated by MAM-derived effectors. Here, we show that in response to inflammasome activators, MAMs localize adjacent to Golgi membranes. Diacylglycerol (DAG) at the Golgi rapidly increases, recruiting protein kinase D (PKD), a key effector of DAG. Upon PKD inactivation, self-oligomerized NLRP3 is retained at MAMs adjacent to Golgi, blocking assembly of the active inflammasome. Importantly, phosphorylation of NLRP3 by PKD at the Golgi is sufficient to release NLRP3 from MAMs, resulting in assembly of the active inflammasome. Moreover, PKD inhibition prevents inflammasome autoactivation in peripheral blood mononuclear cells from patients carrying NLRP3 mutations. Hence, Golgi-mediated PKD signaling is required and sufficient for NLRP3 inflammasome activation.
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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.