炎症体
目标2
促炎细胞因子
NLRP1
分泌物
细胞生物学
半胱氨酸蛋白酶1
多蛋白复合物
细胞外
吡喃结构域
生物
上睑下垂
化学
免疫学
炎症
半胱氨酸蛋白酶
细胞凋亡
遗传学
程序性细胞死亡
生物化学
基因
标识
DOI:10.1016/j.coi.2009.12.004
摘要
In response to injurious or infectious agents caspase-1 activating multiprotein complexes, termed inflammasomes, assemble in the cytoplasm of cells. Activated caspase-1 cleaves the proforms of the interleukin-1 cytokine family members leading to their activation and secretion. The IL-1 family cytokines have multiple proinflammatory activities implicating them in the pathogenesis of many inflammatory diseases. While defined ligands have been identified for the NLRP1, IPAF, and AIM2 inflammasomes, little is known about the activation mechanisms of the NLRP3 inflammasome. Numerous different molecular entities, such as various crystals, pore-forming toxins, or extracellular ATP can trigger the NLRP3 inflammasome. Recent work proposes that NLRP3 is activated indirectly by host factors that are generated in response to NLRP3 triggers.
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