INT81049
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
NCX-4016, but not aspirin, prevented ICE activation as measured by assessing the release of ICE p20 subunit. | |||||||||||||||
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AEA also showed a marked increase of interleukin Ibeta- converting enzyme (ICE)CED-3 family protease (caspase-3) activity. | |||||||||||||||
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AEA also showed a marked increase of interleukin Ibeta- converting enzyme (ICE)CED-3 family protease (caspase-3) activity. | |||||||||||||||
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This effect is largely owing to post-translational nitrosation and therefore inactivation of cysteine proteases, such as the interleukin (IL)-1beta converting enzyme (ICE/caspase-1) involved in pro-cytokine processing. | |||||||||||||||
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Caspase-1, the IL-1beta converting enzyme (ICE), is required for intracellular processing/maturation of IL-1beta and IL-18. | |||||||||||||||
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This leads to activation of N-terminal domain and subsequent PYD-PYD homologous protein interaction leading to the recruitment of the ASC adaptor protein, which together with CARDINAL activates caspase-1, which, in turn cleaves pro-IL-1ß into its active form (Church et al 2008; Martinon et al 2002) (Figure 1). | |||||||||||||||
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It has been proposed that these mutations have a gain of function effect, leading to spontaneous oligorimerization of NALP3 subunits around mutated NACHT domains and subsequent caspase-1 activation resulting in an excessive and inappropriate IL-1? | |||||||||||||||
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When coupled with an increase in IL-1 receptor and ICE with increasing degeneration, the net effect would be the initiation and perpetuation of an IL-1-mediated response. | |||||||||||||||
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The precise mechanism of P2X7 receptor-induced caspase-1 activation is not clear but is known to require K+ efflux and assembly of the NALP3 inflammasome (11, 12). | |||||||||||||||
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When coupled with an increase in IL-1 receptor and ICE with increasing degeneration, the net effect would be the initiation and perpetuation of an IL-1-mediated response. | |||||||||||||||
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Several mechanisms regulate the apoptotic process, such as induction of a p53-dependent-pathway after DNA-damaging agents, modulation by the bcl2 family of proteins, and activation of some effectors including the interleukin-converting enzyme (ICE) family of proteases and endonucleases [24,25]. | |||||||||||||||
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production and release were investigated for dependence upon caspase-1, P2X7 receptor activation, and loss of membrane asymmetry associated with microvesicle shedding. | |||||||||||||||
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We show that human peripheral blood monocytes undergo PS exposure in response to P2X7 receptor activation, which was independent of priming stimulus, caspase-1 activation, and IL-1? | |||||||||||||||
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We also observed that various pro-inflammatory mediators, including cytokines, chemokines, adhesion molecules, prostaglandin E(2) and its key enzyme COX-2, not iNOS or caspase-1, were markedly up-regulated by stimulation with these TLR and NOD agonists. | |||||||||||||||
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IL-1beta-induced NF-kappaB activation was suppressed directly by cocktails of curcumin and resveratrol through inhibition of Ikappakappa and proteasome activation, inhibition of IkappaBalpha phosphorylation and degradation, and inhibition of nuclear translocation of NF-kappaB. | |||||||||||||||
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expression and activation of interleukin-1 converting enzyme (caspase-1). | |||||||||||||||
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expression and activation of interleukin-1 converting enzyme (caspase-1). | |||||||||||||||
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The cryopyrin protein contains an N-terminal pyrin domain and has an important role in regulation of the assembly of the inflammasome, a group of proteins that when assembled activate caspase-1 that cleaves pro IL-1? | |||||||||||||||
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This results in caspase-1 activation and the subsequent processing of pro-interleukin-1-beta to its active form (Trinchieri & Sher 2007). | |||||||||||||||
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In addition to the role of caspases in the regulation and execution of cell death, caspase 1 (also termed IL-converting enzyme) is responsible for converting the precursors of IL-1 family cytokines IL-1? | |||||||||||||||
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