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Details on Person The NLRP3 inflammasome is activated by a range of stimuli of...
| Class:Id | Summation:844607 |
|---|---|
| _displayName | The NLRP3 inflammasome is activated by a range of stimuli of... |
| _timestamp | 2011-04-28 10:27:19 |
| created | [InstanceEdit:844609] Jupe, S, 2010-05-28 |
| literatureReference | [LiteratureReference:873959] The NLRP3 inflammasome: a sensor of immune danger signals [LiteratureReference:874011] Pannexin-1 mediates large pore formation and interleukin-1beta release by the ATP-gated P2X7 receptor [LiteratureReference:873974] Pannexin-1 couples to maitotoxin- and nigericin-induced interleukin-1beta release through a dye uptake-independent pathway [LiteratureReference:874038] Intracellular pattern-recognition receptors [LiteratureReference:873948] Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization [LiteratureReference:874004] The NALP3 inflammasome is involved in the innate immune response to amyloid-beta [LiteratureReference:874054] Mechanisms of caspase-1 activation by P2X7 receptor-mediated K+ release [LiteratureReference:877174] Staphylococcus aureus alpha-hemolysin activates the NLRP3-inflammasome in human and mouse monocytic cells [LiteratureReference:877373] The NOD: a signaling module that regulates apoptosis and host defense against pathogens [LiteratureReference:877384] NODs: intracellular proteins involved in inflammation and apoptosis [LiteratureReference:874016] ATP activates a reactive oxygen species-dependent oxidative stress response and secretion of proinflammatory cytokines in macrophages |
| modified | [InstanceEdit:844626] Jupe, S, 2010-05-28 [InstanceEdit:874056] Jupe, S, 2010-06-09 [InstanceEdit:877211] Jupe, S, 2010-06-11 [InstanceEdit:877317] Jupe, S, 2010-06-11 [InstanceEdit:877366] Jupe, S, 2010-06-14 [InstanceEdit:1250252] Jupe, S, 2011-04-15 [InstanceEdit:1252399] Jupe, S, 2011-04-27 [InstanceEdit:1253356] Jupe, S, 2011-04-28 |
| text | The NLRP3 inflammasome is activated by a range of stimuli of microbial, endogenous and exogenous origins including several viruses, bacterial pore forming toxins (e.g. Craven et al. 2009), and various irritants that form crystalline or particulate structures (see Cassel et al. 2009). Multiple studies have shown that phagocytosis of particulate elicitors is necessary for activation (e.g. Hornung et al. 2008) but not for the response to ATP, which is mediated by the P2X7 receptor (Kahlenberg & Dubyak, 2004) and appears to involve the pannexin membrane channel (Pellegrin & Suprenenant 2006), which is also involved in the response to nigericin and maitotoxin (Pellegrin & Suprenenant 2007). Direct binding of elicitors to NLRP3 has not been demonstrated and the exact process of activation is unclear, though speculated to involve changes in conformation that make available the NACHT domain for oligomerization (Inohara & Nunez 2001, 2003). Three overlapping mechanisms are believed to be involved in NLRP3 activation. ATP stimulates the P2X7 ATP-gated ion channel leading to K+ efflux which appears necessary for NLRP3 inflammasome activation (Kahlenberg & Dubyak 2004, Dostert et al. 2008), and is believed to induce formation of pannexin-1 membrane pores. These pores give direct access of NLPR3 agonists to the cytosol. A second mechanism is the endocytosis of crystalline or particulate structures, leading to damaged lysosomes which release their contents (Hornung et al. 2008, Halle et al. 2008). The third element is the generation of reactive oxygen species (ROS) which activate NLRP3, shown to be a critical step for the activation of caspase-1 following ATP stimulation (Cruz et al. 2007). The source of the ROS is unclear. |
| (summation) | [BlackBoxEvent:844440] NLRP3 activation by elicitor proteins [Homo sapiens] [BlackBoxEvent:1306876] NLRP3 activation by small molecules [Homo sapiens] |
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