NALP3, also named as C1orf7, CIAS1 and PYPAF1, belongs to the NLRP family. NALP3 may function as an inducer of apoptosis. It interacts selectively with ASC and this complex may function as an upstream activator of NF-kappa-B signaling.NALP3 inhibits TNF-alpha induced activation and nuclear translocation of RELA/NF-KB p65. Also inhibits transcriptional activity of RELA. NALP3 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. Defects in NLRP3 are the cause of familial cold autoinflammatory syndrome type 1 (FCAS1) which also known as familial cold urticaria. Defects in NLRP3 are a cause of Muckle-Wells syndrome (MWS) which is urticaria-deafness-amyloidosis syndrome. Defects in NLRP3 are the cause of chronic infantile neurologic cutaneous and articular syndrome (CINCA) which also known as neonatal onset multisystem inflammatory disease (NOMID). The antibody recognizes the C-term of NALP3.
Western Blot:K-562 Cells, 1:200-1:2000; IHC: Human bladder Tissue, 1:20-1:200; IF: HepG2 Cells, 1:10-1:100
Type: Primary
Antigen: NALP3
Clonality: Polyclonal
Clone:
Conjugation: Unconjugated
Epitope:
Host: Rabbit
Isotype: IgG
Reactivity: Human
