ArticleNature communications2016
ASC filament formation serves as a signal amplification mechanism for inflammasomes.
Article in Nature communications, 2016. 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 244 papers.
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Who cites it
244 citing papers in PubMed, 402 citations in OpenAlex.
- Structural insights into human caspase-9 CARD assembly modes driven by conserved arginine hotspots.Journal of structural biology: X · 2026Article
- Exploratory Analysis of Autophagy-related Genes and Immune Infiltration in Human Hippocampal Tissue of Temporal Lobe Epilepsy.Molecular neurobiology · 2026Article
- MyD88 self-assembles into supramolecular filaments to amplify NF-κB signaling.Fundamental research · 2026Article
- RNA helicase DDX6 governs ASC speck formation in P-bodies and the transition to stress granules via phase separation during inflammasome activation.Cell discovery · 2026Article
- OLT1177 (Dapansutrile) inhibits Gasdermin D-dependent IL-1β Release and Pyroptotic Cell Death in Bone Marrow-derived Macrophages.bioRxiv : the preprint server for biology · 2026Article
- Muscone Promotes PINK1/Parkin-Associated Mitophagy to Suppress NLRP3 Inflammasome Activation: Implications for Endotoxemia Therapy.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Inflammasome adaptor protein ASC is a mechanistic checkpoint in IL-1β maturation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- GTPase Rab11b and effector Rab11-FIP2 promote NLRP3 stability during inflammasome priming.The EMBO journal · 2026Article
- [Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Article
- Unravelling the role of PANoptosis in diseases: from emerging molecular mechanisms-to-therapeutic implications.Cancer biology & medicine · 2026Review
- PDK4 drives abdominal aortic aneurysm by promoting smooth muscle cell metabolic reprogramming and NLRP3-mediated pyroptosis.Nature communications · 2026Article
- β-alanine alleviates gout by inhibiting NLRP3 inflammasome activation.Journal of molecular cell biology · 2026Article
- The P2X7 receptor/NLRP3 inflammasome signaling axis in sepsis: molecular mechanisms, organ-specific pathophysiology, and emerging therapeutic strategies.Purinergic signalling · 2026Review
- The NLRP3 Inflammasome: Mechanisms of Activation, Regulation, and Therapeutic Opportunities.MedComm · 2026Review
- Circulating cfdna: A novel biomarker for preventing early recurrence in ischemic stroke.Journal of thrombosis and thrombolysis · 2026Review
- Environmental Amino Acid Sensing Regulates the Rate of ASC Translation and NLRP3 Inflammasome Assembly.bioRxiv : the preprint server for biology · 2026Article
- Disruption of NLRP3 inflammasome assembly via ligand-induced remodeling of pyrin domain interfaces.Scientific reports · 2026Article
- LPS-induced structural reorganization and polymerization drive noncanonical inflammasome activation.Science advances · 2026Article
- The inhibition of the Aβ-ASC interaction site suppresses β-amyloid aggregation and cytotoxicity.Frontiers in immunology · 2026Article
- Old dogs-new tricks: multifaceted functions of MAVS beyond antivirus activity in human health and diseases.Cell & bioscience · 2025Review
184 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A hallmark of inflammasome activation is the ASC speck, a micrometre-sized structure formed by the inflammasome adaptor protein ASC (apoptosis-associated speck-like protein containing a CARD), which consists of a pyrin domain (PYD) and a caspase recruitment domain (CARD). Here we show that assembly of the ASC speck involves oligomerization of ASC(PYD) into filaments and cross-linking of these filaments by ASC(CARD). ASC mutants with a non-functional CARD only assemble filaments but not specks, and moreover disrupt endogenous specks in primary macrophages. Systematic site-directed mutagenesis of ASC(PYD) is used to identify oligomerization-deficient ASC mutants and demonstrate that ASC speck formation is required for efficient processing of IL-1β, but dispensable for gasdermin-D cleavage and pyroptosis induction. Our results suggest that the oligomerization of ASC creates a multitude of potential caspase-1 activation sites, thus serving as a signal amplification mechanism for inflammasome-mediated cytokine production.
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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.