NLRP3
NLRP3 (NLR family pyrin domain containing 3, also known as NALP3, PYPAF1, CIAS1 and CLR1.1) is a pyrin-domain-containing member of the NLRP family. It nucleates the NLRP3 inflammasome, a complex that regulates inflammation, immune responses and apoptosis. Browse Assay Genie's current range of NLRP3 research reagents below, or read on for the biology behind the target.
NLRP3 is a multidomain protein that contains a pyrin domain, a nucleotide-binding site (NBS) domain and a leucine-rich repeat (LRR) motif. It interacts with the apoptosis-associated speck-like protein PYCARD/ASC, which carries a caspase recruitment domain, and is a member of the NLRP3 inflammasome complex. This complex acts as an upstream activator of NF-kappaB signalling and plays a role in the regulation of inflammation, the immune response and apoptosis. The SARS-CoV 3a protein, a transmembrane pore-forming viroporin, has been shown to activate the NLRP3 inflammasome by forming ion channels in macrophages.
Independently of inflammasome activation, NLRP3 regulates the differentiation of T helper 2 (Th2) cells and has a role in Th2 cell-dependent asthma and tumour growth. During Th2 differentiation it is required for optimal IRF4 binding to the IL4 promoter and for IRF4-dependent IL4 transcription. It binds the consensus DNA sequence 5'-GRRGGNRGAG-3' and may also participate in the transcription of IL5, IL13, GATA3, CCR3, CCR4 and MAF. UniProt records the protein in several compartments, including the cytosol, inflammasome, Golgi apparatus membrane, endoplasmic reticulum, mitochondrion and nucleus, and it is also annotated as secreted.
The human NLRP3 gene is also known by the previous names cold autoinflammatory syndrome 1 and deafness, autosomal dominant 34. Mutations are associated with familial cold autoinflammatory syndrome (FCAS), Muckle-Wells syndrome (MWS), chronic infantile neurological cutaneous and articular (CINCA) syndrome, neonatal-onset multisystem inflammatory disease (NOMID), keratoendotheliitis fugax hereditaria, and autosomal dominant deafness 34 with or without inflammation. Multiple alternatively spliced transcript variants encoding distinct isoforms have been identified.
NLRP3 interacts with ASC and forms the NLRP3 inflammasome, making it a central subject in studies of inflammatory signalling and apoptosis.
Mutations in the NLRP3 gene are linked to FCAS, Muckle-Wells syndrome, CINCA and NOMID, so the protein is widely studied in these disorders.
NLRP3 supports IRF4-dependent IL4 transcription during Th2 differentiation and has a role in Th2 cell-dependent asthma and tumour growth.
The SARS-CoV 3a viroporin activates the NLRP3 inflammasome through ion channel formation in macrophages, linking NLRP3 to host responses to viruses.
NLRP3 is a component of the NLRP3 inflammasome, which interacts with ASC (PYCARD) and acts upstream of NF-kappaB signalling to regulate inflammation, immune responses and apoptosis. Separately, it supports Th2 differentiation by promoting IRF4-dependent IL4 transcription.
NLRP3 is also called NALP3, PYPAF1, CIAS1, CLR1.1, C1orf7, FCAS, MWS and DFNA34, among other aliases. Earlier names include cold autoinflammatory syndrome 1. Multiple alternatively spliced transcript variants encoding distinct isoforms have been reported for the gene.
Mutations in NLRP3 are associated with FCAS, Muckle-Wells syndrome, CINCA, NOMID and autosomal dominant deafness 34. Mouse and rat both have an Nlrp3 ortholog; check the datasheet of any product for its validated reactivity.
Other NLRP family members and inflammasome-related targets with products at Assay Genie.
Gene and protein annotations from HGNC, NCBI Gene and UniProt Q96P20; product specifications from Assay Genie datasheets.