The NLRP3 inflammasome & pyroptosis
The NLRP3 inflammasome & pyroptosis. A two-signal platform: Signal 1 (TLR → NF-κB) primes the cell by inducing NLRP3 and the pro-cytokines, while Signal 2 (ATP via P2X7, crystals, K+ efflux) triggers NLRP3 to nucleate ASC and activate caspase-1. Active caspase-1 matures IL-1β and IL-18 and cleaves gasdermin-D to drive pyroptosis. Click any protein for the matching Assay Genie In Vivo functional-grade antibody or ELISA kit.
Signal 1 (priming). Microbial or endogenous ligands engage TLR4, activating NF-κB to transcribe NLRP3 itself plus the inactive precursors pro-IL-1β and pro-IL-18. This step licences the cell but does not yet release cytokine.
Signal 2 (activation). A second stimulus — extracellular ATP through the P2X7 channel, particulate crystals, reactive oxygen species or K+ efflux — activates the sensor NLRP3 (with NEK7). Parallel sensors AIM2 (cytosolic dsDNA) and NLRC4 (flagellin / T3SS) feed the same hub. The sensor recruits the adaptor ASC (PYCARD), which polymerises and clusters pro-caspase-1, driving its autoproteolysis to active caspase-1.
Effector output. Caspase-1 cleaves pro-IL-1β and pro-IL-18 into secreted IL-1β and IL-18, and cleaves gasdermin-D, whose N-terminal fragment perforates the membrane to cause pyroptosis — lytic, inflammatory cell death that releases DAMPs. Assay Genie’s In Vivo functional-grade anti-IL-1β neutralises the key output, with ELISA kits covering every sensor, adaptor and effector. For research use only; not for diagnostic or therapeutic procedures. Mouse targets shown.
Every protein node links to a product: In Vivo anti-IL-1β for the key output; sensors, adaptor, caspase and gasdermin open the matching ELISA kit.