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Human NLRP3 Protein expressed in Wheat germ - ABIN1312675
Lu, Nakamura, Inouye, Li, Tang, Lundbäck, Valdes-Ferrer, Olofsson, Kalb, Roth, Zou, Erlandsson-Harris, Yang, Ting, Wang, Andersson, Antoine, Chavan, Hotamisligil, Tracey: Novel role of PKR in inflammasome activation and HMGB1 release. in Nature 2012
Show all 5 Pubmed References
findings suggest that beside the RLR (show DHX58 Proteins) pathway, RNase L (show RNASEL Proteins) cleavage products can also activate the NLRP3-inflammasome pathway, which requires DHX33 (show DHX33 Proteins) (DExD/H-box helicase) and the mitochondrial adaptor protein MAVS (show MAVS Proteins).
Collectively, our findings show that inhibition of the NLRP3 inflammasome decreases foam cell formation of THP-1 macrophages via suppression of ox-LDL uptake and enhancement of cholesterol efflux, which may be due to downregulation of CD36 (show CD36 Proteins) expression and upregulation of ABCA1 (show ABCA1 Proteins) and SR-BI (show SCARB1 Proteins) expression, respectively.
This review surveys the involvement of the NLRP3 inflammasome in various signalling pathways and highlight different aspects of their influence on diabetic nephropathy. [review]
Data suggest that aggregates of amyloid beta(1-40) induce excessive generation of reactive oxygen species, MAPK (show MAPK1 Proteins)/NFkappaB (show NFKB1 Proteins) signaling activation, and NLRP3 inflammasome activation in retinal pigment epithelial cells mimicking changes seen in age-related macular degeneration; this mechanism is dependent on NADPH oxidase (show NOX1 Proteins).
results indicate a possible role of the NLRP3 inflammasome and its genetic variants in the pathogenesis of atherosclerosis.
Our results show that Tim-3 (show HAVCR2 Proteins) is a critical negative regulator of NLRP3 inflammasome and provides a potential target for intervention of diseases with uncontrolled inflammasome activation.
IL-27 (show IL27 Proteins) increased NLRP3 inflammasome activation in monocytes with enhanced release of IL-1 beta (show IL1B Proteins).
Study shows NLRP3 functionally replaces AIM2 (show AIM2 Proteins) as the bona-fide DNA inflammasome sensor in human myeloid cells. As opposed to AIM2 (show AIM2 Proteins), which directly binds to DNA, NLRP3 is hardwired to the upstream DNA-sensing cGAS-STING pathway to trigger inflammasome activation.
sickle red blood cell induced TLR9 (show TLR9 Proteins), NLRP3, Caspase-1 (show CASP1 Proteins), IL-1beta (show IL1B Proteins) and IL-18 (show IL18 Proteins) expression and induced IL-1beta (show IL1B Proteins), LTB4 (show PTGR1 Proteins) and nitrite production in PBMC cultures.
some molecules such as JNK-1 (show MAPK8 Proteins) and ASK-1 (show MAP3K5 Proteins) can reduce atherosclerosis through inducing apoptosis in macrophages. Notably, NLRP3 inflammasome can also cause apoptosis in macrophages, suggesting that NLRP3 inflammasome may mediate JNK (show MAPK8 Proteins)-induced apoptosis. the role of NLRP3 in atherogenesis can be significant.
Data suggest that advanced glycation end products act on bone marrow-derived macrophages to impair Nlrp3 inflammasome-mediated innate immunity.
blockade of RAGE (show AGER Proteins) inhibited AGE-RAGE (show AGER Proteins)-induced ROS (show ROS1 Proteins) production and attenuated TXNIP (show TXNIP Proteins)-NLRP3 activation, thus reducing the levels of the pro-inflammatory cytokine IL-1beta (show IL1B Proteins) and consequently attenuating abnormal kidney function and vascular endothelial dysfunction
In the absence of NLRP3 inflammasome, prolonged stress does not provoke depressive behavior or microglial activation compared to controls.
NLRP3 inflammasome activation in HSCs may serve as an early mechanism to turn on the inflammatory response and thereby instigate liver fibrosis during Schistosoma J infection
Nlrp3 regulated caspase-8 (show CASP8 Proteins) activation downstream of multiple pathways involving TNFR (show TNFRSF1A Proteins), CD95 (show FAS Proteins) and non-death receptor apoptosis triggered by etoposide. Second, the impact of K+ on epithelial cell apoptosis and the formation of the non-canonical NLRP3/ASC (show STS Proteins)/caspase-8 (show CASP8 Proteins) platform implies that multiple mitochondrial cell death pathways may converge on a single mechanism to that involving NLRP3.
sestrin2 has a role in suppressing sepsis by inducing mitophagy and inhibiting NLRP3 activation in macrophages
the agonists inhibited the priming of inflammasome activation. In vivo data also showed that LXRs agonist prevented NLRP3-dependent peritonitis. In conclusion, LXRs agonists are identified to potently suppress NLRP3 inflammasome and the regulation of LXRs signaling is a potential therapeutic for inflammasome-driven diseases.
The reactive oxygen species-dependent activation of endothelial Nlrp3 inflammasomes by hyperglycemia may be an important initiating mechanism to cause endothelial dysfunction.
SGLT-2 (show SLC5A2 Proteins) inhibition with dapagliflozin reduces the activation of the Nlrp3/ASC (show STS Proteins) inflammasome and attenuates the development of diabetic cardiomyopathy in mice with type 2 diabetes. Effects are augmentated of the by DPP4 (show DPP4 Proteins) inhibitor Saxagliptin.
Data show that activated protein C (show PROC Proteins) (aPC (show APC Proteins)) inhibited Nlrp3 inflammasome activation via mammalian target of rapamycin (show FRAP1 Proteins) complex 1 (mTORC1) signaling.
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