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Details on Person The NLRP3 (Cryopyrin) inflammasome is currently the best cha...
| Class:Id | Summation:844622 |
|---|---|
| _displayName | The NLRP3 (Cryopyrin) inflammasome is currently the best cha... |
| _timestamp | 2011-04-15 16:03:58 |
| created | [InstanceEdit:844609] Jupe, S, 2010-05-28 |
| literatureReference | [LiteratureReference:844443] The inflammasomes [LiteratureReference:873966] CATERPILLERs, pyrin and hereditary immunological disorders [LiteratureReference:873948] Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization [LiteratureReference:874054] Mechanisms of caspase-1 activation by P2X7 receptor-mediated K+ release [LiteratureReference:874011] Pannexin-1 mediates large pore formation and interleukin-1beta release by the ATP-gated P2X7 receptor [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 |
| modified | [InstanceEdit:844626] Jupe, S, 2010-05-28 [InstanceEdit:874056] Jupe, S, 2010-06-09 [InstanceEdit:877211] Jupe, S, 2010-06-11 [InstanceEdit:877366] Jupe, S, 2010-06-14 [InstanceEdit:879225] Jupe, S, 2010-06-15 [InstanceEdit:918254] Jupe, S, 2010-08-02 [InstanceEdit:1250252] Jupe, S, 2011-04-15 |
| text | The NLRP3 (Cryopyrin) inflammasome is currently the best characterized. It consists of NLRP3, ASC (PYCARD) and procaspase-1; CARD8 (Cardinal) is also suggested to be a component. It is activated by a number of pathogens and bacterial toxins as well as diverse PAMPs, danger-associated molecular patterns (DAMPS) such as hyaluronan and uric acid, and exogenous irritants such as silica and asbestos (see Table S1 Schroder & Tschopp, 2010). Mutations in NLRP3 which lead to constitutive activation are linked to the human diseases Muckle-Wells syndrome, familial cold autoinflammatory syndrome and NOMID (Ting et al. 2006), characterized by skin rashes and other symptoms associated with generalized inflammation. The cause of these symptoms is uncontrolled IL-1 beta production. Multiple studies have shown that activation of the NLRP3 inflammasome by particulate activators (e.g. Hornung et al. 2008) requires phagocytosis, but this is not required 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). Direct binding of activators to NLRP3 has not been demonstrated and the exact process of activation is unclear, though it is speculated to involve changes in conformation that free the NACHT domain for oligomerization (Inohara & Nunez 2001, 2003). |
| (summation) | [Pathway:844456] The NLRP3 inflammasome [Homo sapiens] |
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