Anti-CIAS1/NALP3/NLRP3 Antibody Picoband® Fluoro647 Conjugated

NLRP3 (NLR FAMILY, PYRIN DOMAIN-CONTAINING 3), also known as CIAS1, CRYOPYRIN, NALP3 or PYPAF1, is a protein that in humans is encoded by the NLRP3 gene. It is mapped to 1q44. The encoded protein may play a role in the regulation of inflammation and apoptosis. Mutation of the NALP3 nucleotide-binding domain reduced ATP binding, CASP1 activation, IL1B production, cell death, macromolecular complex formation, self-association, and association with ASC. Consistent with an essential role for Nlrp3 inflammasomes in antifungal immunity, it has been showed that Nlrp3-deficient mice are hypersusceptible to C. albicans infection. Activation of the NLRP3 inflammasome in response to virus or to RNA was dependent upon lysosomal maturation and reactive oxygen species production in human cells. The NLRP3 inflammasome senses obesity-associated danger signals and contributes to obesity-induced inflammation and insulin resistance.

NACHT, LRR and PYD domains-containing protein 3; Angiotensin/vasopressin receptor AII/AVP-like; Caterpiller protein 1.1; CLR1.1; Cold autoinflammatory syndrome 1 protein; Cryopyrin; PYRIN-containing APAF1-like protein 1; NLRP3; C1orf7, CIAS1, NALP3, PYPAF1

Expressed in blood leukocytes. Strongly expressed in polymorphonuclear cells and osteoblasts. Undetectable or expressed at a lower magnitude in B- and T-lymphoblasts, respectively. High level of expression detected in chondrocytes. Detected in non-keratinizing epithelia of oropharynx, esophagus and ectocervix and in the urothelial layer of the bladder. .

Apoptosis, Associated Proteins, Atherosclerosis, Cancer, Cardiovascular, Cell Biology, Growth Factors, Immunology, Innate Immunity, Intracellular, Macrophage/Inflammation, NFKB Pathway, Nuclear Signaling, Signal Transduction, Signaling Pathway, Vascular Inflammation

May function as an inducer of apoptosis. Interacts selectively with ASC and this complex may function as an upstream activator of NF-kappa-B signaling. Inhibits TNF-alpha induced activation and nuclear translocation of RELA/NF-KB p65. Also inhibits transcriptional activity of RELA. Activates caspase-1 in response to a number of triggers including bacterial or viral infection which leads to processing and release of IL1B and IL18. .

1. Agostini, L., Martinon, F., Burns, K., McDermott, M. F., Hawkins, P. N., Tschopp, J. NALP3 forms an IL-1-beta-processing inflammasome with increased activity in Muckle-Wells autoinflammatory disorder. 2. Allen, I. C., Scull, M. A., Moore, C. B., Holl, E. K., McElvania-TeKippe, E., Taxman, D. J., Guthrie, E. H., Pickles, R. J., Ting, J. P.-Y. The NLRP3 inflammasome mediates in vivo innate immunity to influenza A virus through recognition of viral RNA. Immunity 30: 556-565, 2009. 3. Hoffman HM, Wright FA, Broide DH, Wanderer AA, Kolodner RD (Jun 2000) . Identification of a locus on chromosome 1q44 for familial cold urticaria. Am J Hum Genet 66 (5) : 1693–8.