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Mouse (Murine) NLRP3 ELISA Kit for Sandwich ELISA - ABIN818941
Kleiner, Celsi, Tricarico, Zacchigna, Crovella, Marcuzzi: Systemic and neuronal inflammatory markers in a mouse model of mevalonate kinase deficiency: a strain-comparative study. in In vivo (Athens, Greece) 2013
Human NLRP3 ELISA Kit for Sandwich ELISA - ABIN857854
Piippo, Korkmaz, Hytti, Kinnunen, Salminen, Atalay, Kaarniranta, Kauppinen: Decline in cellular clearance systems induces inflammasome signaling in human ARPE-19 cells. in Biochimica et biophysica acta 2014
Patients with low-penetrance NLRP3 variants display a distinct clinical phenotype and an intermediate biologic phenotype, including IL-1beta (show IL1B ELISA Kits) and non-IL-1beta (show IL1B ELISA Kits)-mediated inflammatory pathway activation.
the association of TXNIP (thioredoxin-interacting protein (show TXNIP ELISA Kits)) with NLRP3 induced by ROS (show ROS1 ELISA Kits) promoted NLRP3 inflammasome activation in senescent HUVEC endothelial cells
these findings are the first to identify NLRP3 as an inflammasome sensor for Toxoplasma gondii in primary human peripheral blood cells and to define an upstream regulator of its activation through the release of intracellular potassium
Stress-Induced NLRP3 inflammasome complex emerges as an important factor in the pathogenesis and progression of human diseases. [review]
that NLRP3 may have specific function in the spiral ganglion neurons and can be associated with both syndromic and nonsyndromic sensorineural deafness
results firstly revealed that irisin (show FNDC5 ELISA Kits) mitigated oxygen-glucose deprivation-induced neuronal injury in part via inhibiting ROS (show ROS1 ELISA Kits)-NLRP3 inflammatory signaling pathway, suggesting a likely mechanism for irisin (show FNDC5 ELISA Kits)-induced therapeutic effect in ischemic stroke.
Anti-dsDNA Abs activated NLRP3 inflammasome in monocytes/macrophages from systemic lupus erythematosus patients by binding to TLR4 (show TLR4 ELISA Kits) and inducing the production of mitochondrial reactive oxygen species.
that miR (show MLXIP ELISA Kits)-20b could alleviate the inflammatory response in Tuberculosis mice via targeting the NLRP3/caspase-1 (show CASP1 ELISA Kits)/IL-1beta (show IL1B ELISA Kits) pathway
level of TGF-beta1 (show TGFB1 ELISA Kits) was reduced after NLRP3 silencing. These results indicated that the NLRP3 inflammasome was activated in alveolar epithelial cells
SNPs in NLRP3 and CTSB (show CTSB ELISA Kits), associated with an increased NLRP3-inflammasome activation, are protective against the development of active pulmonary tuberculosis.
NLRP3-/- mice exhibited resistance to indomethacin-induced small intestinal damage
MiR (show MLXIP ELISA Kits)-133b suppresses Nlrp3 inflammasome activation in nasal mucosa of Allergic Rhinitis mice.
these data are the first to show dramatic posttranscriptional control of inflammatory cytokine production by a relevant tissue-derived macrophage population and proteasomal degradation of proIL-1beta and NLRP3 as a mechanism to control inflammasome activation
Hemorrhagic shock primes for lung vascular endothelial cell pyroptosis following lipopolysaccharide exposure through TLR4 (show TLR4 ELISA Kits), which activates Nlrp3, and subsequently induces caspase-1 (show CASP1 ELISA Kits) activation.
Nlrp3 knock out significantly diminished the quantity of cleaved-Caspase-1 (show CASP1 ELISA Kits).
P50 (show LSP1 ELISA Kits) could interact with NLRP3 inflammasome in MCs (show SMCP ELISA Kits).
JNK1 (show MAPK8 ELISA Kits)-mediated NLRP3 phosphorylation at S194 is a critical priming event and is essential for NLRP3 inflammasome activation.
Carbon monoxide regulates glycolysis-dependent NLRP3 inflammasome activation. Carbon monoxide suppresses the activation of glycolysis. Carbon monoxide prevents hyperglycemia-induced inflammation in vivo.
It was concluded that the HFD-instigated Nrp1 (show NRP1 ELISA Kits) reduction in macrophages exacerbates insulin (show INS ELISA Kits) resistance by promoting Nlrp3 inflammasome priming and activation.
This gene encodes a pyrin-like protein containing a pyrin domain, a nucleotide-binding site (NBS) domain, and a leucine-rich repeat (LRR) motif. This protein interacts with the apoptosis-associated speck-like protein PYCARD/ASC, which contains a caspase recruitment domain, and is a member of the NALP3 inflammasome complex. This complex functions as an upstream activator of NF-kappaB signaling, and it plays a role in the regulation of inflammation, the immune response, and apoptosis. Mutations in this gene are associated with familial cold autoinflammatory syndrome (FCAS), Muckle-Wells syndrome (MWS), chronic infantile neurological cutaneous and articular (CINCA) syndrome, and neonatal-onset multisystem inflammatory disease (NOMID). Multiple alternatively spliced transcript variants encoding distinct isoforms have been identified for this gene. Alternative 5' UTR structures are suggested by available data\; however, insufficient evidence is available to determine if all of the represented 5' UTR splice patterns are biologically valid.
NACHT, LRR and PYD domains-containing protein 3
, cold autoinflammatory syndrome 1
, NLR family, pyrin domain containing 3
, NACHT, LRR and PYD domains-containing protein 3-like
, NACHT domain-, leucine-rich repeat-, and PYD-containing protein 3
, NACHT, LRR and PYD containing protein 3
, PYRIN-containing APAF1-like protein 1
, caterpiller protein 1.1
, cold autoinflammatory syndrome 1 protein
, nucleotide-binding oligomerization domain, leucine rich repeat and pyrin domain containing 3
, NACHT/LRR/pyrin domain-containing protein 3
, cold autoinflammatory syndrome 1 homolog
, cold autoinflammatory syndrome 1 protein homolog
, mast cell maturation inducible protein 1
, mast cell maturation-associated-inducible protein 1
, NLR family pyrin domain containing 3