Thiol protease which cleaves IL-1 beta (il1b), releasing the mature cytokine which is involved in a variety of inflammatory processes, and mediates apoptosis (PubMed:12464617, PubMed:30150286). Component of the NLRP1 inflammasome, which plays a crucial role in innate immunity and inflammation (PubMed:30150286). In response to pathogens and other damage-associated signals, recruited to the NLRP1 inflammasome in its precursor form following the recruitment of caspase caspa (PubMed:30150286). Its subsequent activation causes the cleavage of the midformed pro-il1b and results in il1b maturation and secretion in the extracellular milieu (PubMed:30150286). Activated by direct binding to bacterial lipopolysaccharides (LPS), which causes non-canonical inflammasome activation and results in the pyroptosis of infected cells and their extrusion into the gut lumen, as well as in cytokine secretion (PubMed:30076291). Plays a crucial role in the restriction of bacterial infection to intestinal sites (PubMed:30076291). Pyroptosis limits bacterial replication, while cytokine secretion promotes the recruitment and activation of immune cells and triggers mucosal inflammation (By similarity). Promotes pyroptosis by bacterial infection by E.piscicida (PubMed:30076291). Strict requirement for Asp at the P1 position. It has a preferred cleavage sequence of Tyr-Val-Ala-Asp-|- but also cleaves at Asp-Glu-Val-Asp-|-. Activated by homooligomerization induced by direct binding to cytosolic LPS. Upon direct LPS-binding, forms large homooligomers, resulting in its activation (PubMed:30076291). These oligomers are often referred to as 'non-canonical inflammasomes' (PubMed:30076291). Heterotetramer that consists of two anti-parallel arranged heterodimers, each one formed by a 20 kDa (p20) and a 10 kDa (p10) subunit (Probable). Interacts with caspa (PubMed:29791979). Interacts with pycard; the interaction only occurs in the presence of nlrp1 (PubMed:30150286). Component of NLRP1 inflammasomes (PubMed:30150286). Inflammasomes are supramolecular complexes that assemble in the cytosol in response to pathogens and other damage-associated signals and play critical roles in innate immunity and inflammation (PubMed:30150286). The NLRP1 inflammasome is composed of the signal sensor nlrp1, and the adapter pycard (asc), which recruit effector pro-inflammatory caspases caspa and/or caspb (PubMed:30150286). The interaction between nlrp1 and pycard is required for the sequential recruitment of caspa and then caspb (PubMed:30150286). Caspa is preferentially recruited first and this causes the cleavage of pro-il1b into the midformed il1b (PubMed:30150286). This is followed by the recruitment of caspb, which is activated and cleaves the midformed il1b resulting in il1b maturation (PubMed:30150286). Co-localizes with pycard, caspa and nlrp1 in the cytoplasm (PubMed:30150286). Co-localizes with pycard at large cytoplasmic aggregates, known as specks (PubMed:30150286). Expressed in the spleen, kidney and liver, and highly expressed in the gills and gut. During embryonic development, highly expressed at 8 hours post-fertilization (hpf) (PubMed:28402832). Expressed at the pharyngula stage at 24 hpf and expression is maintained for 7 days post-fertilization (PubMed:29791492, PubMed:28402832, PubMed:30076291). During this time, expressed in the pharyngeal arches, and in the epidermis and proctoderm at 48 hpf, and in the epidermis at 72 hpf (PubMed:29791492, PubMed:12464617, PubMed:30076291). Also expressed in the mouth at 48 and 72 hpf (PubMed:12464617, PubMed:30076291). Up-regulated in response to pentachlorophenol (PCP), a toxic pollutant (PubMed:28402832). Up-regulated in response to bacterial lipopolysaccharides (LPS) and bacterial infection with E.piscicida (PubMed:30076291). Up-regulated in response to bacterial infection with E.tarda (PubMed:30150286). The Pyrin domain mediates LPS recognition and homooligomerization. The two subunits are derived from the precursor sequence by an autocatalytic mechanism. Impaired pyroptosis in response to bacterial infection with E.piscicida (PubMed:30076291). Morpholino knockdown results in no observed phenotype (PubMed:30076291). Morpholino knockdown results in impaired gut bacterial clearance following bacterial infection with E.piscicida (PubMed:30076291). Morpholino knockdown results in pericardial edema, erosion of the tail fin and body axis, and impaired up-regulation of il1b, tnfa, il6, il8, il10 and ifng1 cytokines in response to bacterial lipopolysaccharides (LPS) (PubMed:30076291). Belongs to the peptidase C14A family.