Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
Mutation of a new gene encoding a putative pyrin-like protein causes familial cold autoinflammatory syndrome and Muckle-Wells syndrome.
PYPAF1, a PYRIN-containing Apaf1-like protein that assembles with ASC and regulates activation of NF-kappa B.
[Profanities and the profane person].
Chronic infantile neurological cutaneous and articular syndrome is caused by mutations in CIAS1, a gene highly expressed in polymorphonuclear cells and chondrocytes.
A novel PAAD-containing protein that modulates NF-kappa B induction by cytokines tumor necrosis factor-alpha and interleukin-1beta.
De novo CIAS1 mutations, cytokine activation, and evidence for genetic heterogeneity in patients with neonatal-onset multisystem inflammatory disease (NOMID): a new member of the expanding family of pyrin-associated autoinflammatory diseases.
Cutting edge: CIAS1/cryopyrin/PYPAF1/NALP3/CATERPILLER 1.1 is an inducible inflammatory mediator with NF-kappa B suppressive properties.
Cryopyrin-induced interleukin 1beta secretion in monocytic cells: enhanced activity of disease-associated mutants and requirement for ASC.
NALP3 forms an IL-1beta-processing inflammasome with increased activity in Muckle-Wells autoinflammatory disorder.
PYPAF3, a PYRIN-containing APAF-1-like protein, is a feedback regulator of caspase-1-dependent interleukin-1beta secretion.
NLRs join TLRs as innate sensors of pathogens.
Gout-associated uric acid crystals activate the NALP3 inflammasome.
Hearing improvement in a patient with variant Muckle-Wells syndrome in response to interleukin 1 receptor antagonism.
Inflammasome components NALP 1 and 3 show distinct but separate expression profiles in human tissues suggesting a site-specific role in the inflammatory response.
Phenotype, genotype, and sustained response to anakinra in 22 patients with autoinflammatory disease associated with CIAS-1/NALP3 mutations.
Cryopyrin/NALP3 binds ATP/dATP, is an ATPase, and requires ATP binding to mediate inflammatory signaling.
Innate immune activation through Nalp3 inflammasome sensing of asbestos and silica.
Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization.
AIM2 recognizes cytosolic dsDNA and forms a caspase-1-activating inflammasome with ASC.
Evaluation of Nod-like receptor (NLR) effector domain interactions.
A role for mitochondria in NLRP3 inflammasome activation.
Inflammasomes in health and disease.
GBP5 promotes NLRP3 inflammasome assembly and immunity in mammals.
Novel role of PKR in inflammasome activation and HMGB1 release.
Cell volume regulation modulates NLRP3 inflammasome activation.
Human respiratory syncytial virus viroporin SH: a viral recognition pathway used by the host to signal inflammasome activation.
The adaptor MAVS promotes NLRP3 mitochondrial localization and inflammasome activation.
Omega-3 fatty acids prevent inflammation and metabolic disorder through inhibition of NLRP3 inflammasome activation.
The DHX33 RNA helicase senses cytosolic RNA and activates the NLRP3 inflammasome.
The PYRIN domain-only protein POP3 inhibits ALR inflammasomes and regulates responses to infection with DNA viruses.
Unified polymerization mechanism for the assembly of ASC-dependent inflammasomes.
The NLRP3 inflammasome is released as a particulate danger signal that amplifies the inflammatory response.
ADP-ribosylation of NLRP3 by Mycoplasma pneumoniae CARDS toxin regulates inflammasome activity.
A small-molecule inhibitor of the NLRP3 inflammasome for the treatment of inflammatory diseases.
The receptor NLRP3 is a transcriptional regulator of TH2 differentiation.
TRIM-mediated precision autophagy targets cytoplasmic regulators of innate immunity.
Corrigendum: The receptor NLRP3 is a transcriptional regulator of TH2 differentiation.
Gasdermin D is an executor of pyroptosis and required for interleukin-1β secretion.
NEK7 is an essential mediator of NLRP3 activation downstream of potassium efflux.
NLRP3 tyrosine phosphorylation is controlled by protein tyrosine phosphatase PTPN22.
ASC Pyrin Domain Self-associates and Binds NLRP3 Protein Using Equivalent Binding Interfaces.
Periodic Fever with Aphthous Stomatitis, Pharyngitis, and Cervical Adenitis Syndrome Is Associated with a CARD8 Variant Unable To Bind the NLRP3 Inflammasome.
A Novel Mutation in the Pyrin Domain of the NOD-like Receptor Family Pyrin Domain Containing Protein 3 in Muckle-Wells Syndrome.
NLRP1 promotes tumor growth by enhancing inflammasome activation and suppressing apoptosis in metastatic melanoma.
NLRP3 inflammasome assembly is regulated by phosphorylation of the pyrin domain.
MARK4 regulates NLRP3 positioning and inflammasome activation through a microtubule-dependent mechanism.
NLRP3 mutation and cochlear autoinflammation cause syndromic and nonsyndromic hearing loss DFNA34 responsive to anakinra therapy.
NLRP3 Phosphorylation Is an Essential Priming Event for Inflammasome Activation.
Tyrosine phosphatase SHP2 negatively regulates NLRP3 inflammasome activation via ANT1-dependent mitochondrial homeostasis.
Loss-of-function CARD8 mutation causes NLRP3 inflammasome activation and Crohn's disease.
PtdIns4P on dispersed trans-Golgi network mediates NLRP3 inflammasome activation.
MCC950 directly targets the NLRP3 ATP-hydrolysis motif for inflammasome inhibition.
MCC950 closes the active conformation of NLRP3 to an inactive state.
Structural mechanism for NEK7-licensed activation of NLRP3 inflammasome.
SARS-Coronavirus Open Reading Frame-8b triggers intracellular stress pathways and activates NLRP3 inflammasomes.
Expression of a PYCARD/ASC variant lacking exon 2 in Japanese patients with palindromic rheumatism increases interleukin-1β secretion.
Interactome Mapping Provides a Network of Neurodegenerative Disease Proteins and Uncovers Widespread Protein Aggregation in Affected Brains.
Inflammasomes are activated in response to SARS-CoV-2 infection and are associated with COVID-19 severity in patients.
SARS-CoV-2 N protein promotes NLRP3 inflammasome activation to induce hyperinflammation.
The E3 Ubiquitin Ligase TRIM65 Negatively Regulates Inflammasome Activation Through Promoting Ubiquitination of NLRP3.
BTK operates a phospho-tyrosine switch to regulate NLRP3 inflammasome activity.
Lonicerin targets EZH2 to alleviate ulcerative colitis by autophagy-mediated NLRP3 inflammasome inactivation.
NLRP3 phosphorylation in its LRR domain critically regulates inflammasome assembly.
Structure of the NLRP3 decamer bound to the cytokine release inhibitor CRID3.
Structural basis for the oligomerization-mediated regulation of NLRP3 inflammasome activation.
Directionality of PYD filament growth determined by the transition of NLRP3 nucleation seeds to ASC elongation.
Cryo-EM structures of the active NLRP3 inflammasome disc.
Truncating NFKB1 variants cause combined NLRP3 inflammasome activation and type I interferon signaling and predispose to necrotizing fasciitis.
Consecutive palmitoylation and phosphorylation orchestrates NLRP3 membrane trafficking and inflammasome activation.
ABHD8 antagonizes inflammation by facilitating chaperone-mediated autophagy-mediated degradation of NLRP3.
Non-decameric NLRP3 reveals a TGN/MTOC-distal pathway of inflammasome activation.
The centrosomal hub unifies regulatory factors of NLRP3 inflammasome activation.
NLRP3 oligomerizes via NACHT domains
NLRP3 activation by small molecules
BRISC complex deubiquitinates NLRP3
NLRP3 activation by elicitor proteins
NLRP3 recruits PYCARD (ASC) via a PYD-PYD interaction
PYCARD recruits procaspase-1 via CARD
SGT1:HSP90 binds inactive NLRP3
SARS-CoV-1 8b binds NLRP3
SARS-CoV-1 3a binds TRAF3 within NLRP3 inflammasome