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NLRP3 encodes a pyrin-like protein containing a pyrin domain, a nucleotide-binding site (NBS) domain, and a leucine-rich repeat (LRR) motif. Additionally we are shipping NLRP3 Kits (6) and NLRP3 Proteins (4) and many more products for this protein.
Showing 10 out of 187 products:
Human Polyclonal NLRP3 Primary Antibody for IF (p), IHC (p) - ABIN1386361
Zendedel, Johann, Mehrabi, Joghataei, Hassanzadeh, Kipp, Beyer: Activation and Regulation of NLRP3 Inflammasome by Intrathecal Application of SDF-1a in a Spinal Cord Injury Model. in Molecular neurobiology 2015
Show all 2 references for ABIN1386361
Human Polyclonal NLRP3 Primary Antibody for ICC, IF - ABIN2506713
Saitoh, Tsutsumi, Tada, Ikeda, Noguchi: Recurrent primary leptomeningeal astrocytoma of the lumbosacral spinal cord resembling schwannoma. A case report. in Acta pathologica japonica 1989
Show all 2 references for ABIN2506713
Human Polyclonal NLRP3 Primary Antibody for IHC (p), WB - ABIN652504
Jhang, Lu, Ho, Cheng, Yen: Protective Effects of Catechin against Monosodium Urate-Induced Inflammation through the Modulation of NLRP3 Inflammasome Activation. in Journal of agricultural and food chemistry 2015
Show all 2 references for ABIN652504
Human Polyclonal NLRP3 Primary Antibody for ELISA, WB - ABIN184887
Hoffman, Mueller, Broide, Wanderer, Kolodner: Mutation of a new gene encoding a putative pyrin-like protein causes familial cold autoinflammatory syndrome and Muckle-Wells syndrome. in Nature genetics 2001
Human Polyclonal NLRP3 Primary Antibody for IHC, ELISA - ABIN185676
Kanneganti, Ozören, Body-Malapel, Amer, Park, Franchi, Whitfield, Barchet, Colonna, Vandenabeele, Bertin, Coyle, Grant, Akira, Núñez: Bacterial RNA and small antiviral compounds activate caspase-1 through cryopyrin/Nalp3. in Nature 2006
Human Polyclonal NLRP3 Primary Antibody for EIA, WB - ABIN453768
Feldmann, Prieur, Quartier, Berquin, Certain, Cortis, Teillac-Hamel, Fischer, de Saint Basile: Chronic infantile neurological cutaneous and articular syndrome is caused by mutations in CIAS1, a gene highly expressed in polymorphonuclear cells and chondrocytes. in American journal of human genetics 2002
we propose that the NLRP3 rs10754558 polymorphism contributes to the development of type 2 diabetes mellitus but that rs7512998 and rs12137901 variants are not associated with susceptibility to this disease.
In patients with Age-Related Macular Degeneration increased mRNA levels of NLRP3 are observed.
The proteins of NLRP3, ASC (show PYCARD Antibodies), and caspase-1 (show CASP1 Antibodies) were observed in infiltrating inflammatory cells in cholesteatoma and chronic otitis media.
Necrotic trophoblastic debris induced endothelial cell activation through the IL-1beta (show IL1B Antibodies)/IL-1R pathway. However, the NALP3 inflammasome in endothelial cells was not involved in this process.
Uropathogenic Escherichia coli activates an NLRP3-independent cell death pathway and an aalpha-hemolysin-independent IL-1beta secretion (show IL1B Antibodies)pathway in human macrophages.
NLRP3 gene rs10754558 polymorphisms are associated with increased risk of metabolic syndrome
Findings suggest that immune-activation in the frontal cortex may occur both in patients with bipolar disorderand schizophrenia, while complex I dysfunction and NLRP3-inflammasome activation may be more specific to bipolar disorder
we found no significant association between NALP3 gene polymorphisms and the risk of primary gout.
NLRP3 inflammasome in subcutaneous adipose tissue may have a role in atherogenesis
NLRP3 polymorphism may have a role in diabetic macrovascular complications, especially in myocardial infarction
Same molecule but different expression: aging and sepsis trigger NLRP3 inflammasome activation, a target of melatonin.
AUthors demonstrated, for the first time, that gammaT3 inhibits the NLRP3 inflammasome thereby delaying the progression of type 2 diabetes.
diabetes-associated chronic inflammatory response may have contributed to impaired socket wound healing and rendered oral wound susceptible to the development of bisphosphonate-related osteonecrosis of the jaw via NLRP3 activation in macrophages
Dietary manipulation evokes a maladaptive response in heart mice, as demonstrated by the shift of myosin heavy chain isoform content from alpha to beta, the increased expression of the Nlrp3 inflammasome and markers of oxidative metabolism.
Chronic obstructive pulmonary disease and NLRP3 knockout mice were 5.0 +/- 1.0%, 78.1 +/- 9.2% and 2.0 +/- 0.9%, respectively
NLRP3 was involved in BU/CY-induced liver inflammation after HSCT and selectively inhibited it ameliorated liver inflammation and improved liver function, suggesting targeting NLRP3 might be a new approach in the prophylaxis of liver inflammation
In mouse macrophages, uropathogenic Escherichia coli-triggered inflammasome responses are completely NLRP3-dependent, triggered IL-1beta (show IL1B Antibodies) secretion, and were largely alpha-hemolysin (show PLC Antibodies)-dependent.
enhanced ERK (show EPHB2 Antibodies) signaling in Drp1 (show CRMP1 Antibodies)-knockdown macrophages is implicated in the potentiation of NLRP3 inflammasome activation, via mediating mitochondrial localization of NLRP3 to facilitate the assembly of NLRP3 inflammasome
studies have uncovered the combined actions of the NLRP3 inflammasome and caspase 8 (show CASP8 Antibodies) leading to IL-1beta (show IL1B Antibodies) maturation and the directionality of IL-1beta (show IL1B Antibodies) in driving disease inPstpip2(cmo (show PSTPIP2 Antibodies))mice.
The data reveal that Nlrp3 inflammasome-dependent IL-1beta (show IL1B Antibodies), associated with localized neutrophil recruitment, plays a crucial role in the development of a nonhealing form of cutaneous leishmaniasis in conventionally resistant mice.
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