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Details on Person Interleukin-1β (IL-1β) lacks signal sequences for compartmen...
| Class:Id | Summation:449056 |
|---|---|
| _displayName | Interleukin-1β (IL-1β) lacks signal sequences for compartmen... |
| _timestamp | 2021-02-19 22:03:49 |
| created | [InstanceEdit:449061] Jupe, S, 2009-11-27 |
| literatureReference | [LiteratureReference:9657740] Mechanisms of interleukin-1beta release [LiteratureReference:9657749] The secretion of IL-1β and options for release [LiteratureReference:449024] Nonclassical IL-1 beta secretion stimulated by P2X7 receptors is dependent on inflammasome activation and correlated with exosome release in murine macrophages [LiteratureReference:9657754] Temporal interleukin-1beta secretion from primary human peripheral blood monocytes by P2X7-independent and P2X7-dependent mechanisms [LiteratureReference:9657743] Phospholipases C and A2 control lysosome-mediated IL-1 beta secretion: Implications for inflammatory processes [LiteratureReference:9657750] Essential role for Ca2+ in regulation of IL-1beta secretion by P2X7 nucleotide receptor in monocytes, macrophages, and HEK-293 cells [LiteratureReference:451686] Rapid secretion of interleukin-1beta by microvesicle shedding [LiteratureReference:9657730] Progressive waves of IL-1β release by primary human monocytes via sequential activation of vesicular and gasdermin D-mediated secretory pathways [LiteratureReference:9657721] The unconventional secretion of IL-1β: Handling a dangerous weapon to optimize inflammatory responses [LiteratureReference:9716227] FADD and caspase-8 mediate priming and activation of the canonical and noncanonical Nlrp3 inflammasomes [LiteratureReference:9716256] NLRP3 inflammasome plays a redundant role with caspase 8 to promote IL-1β-mediated osteomyelitis |
| modified | [InstanceEdit:449065] Jupe, S, 2009-11-27 [InstanceEdit:617369] Jupe, S, 2010-04-21 [InstanceEdit:9657722] Shamovsky, Veronica, 2019-08-09 [InstanceEdit:9716268] Shamovsky, Veronica, 2021-02-19 |
| text | Interleukin-1β (IL-1β) lacks signal sequences for compartmentation within the Golgi and classical secretory vesicles, so release of the mature form to extracellular compartments requires nonclassical mechanisms of secretion which are poorly understood (Eder C 2009; Piccioli P & Rubartelli A 2013). Several secretory pathways were proposed involving secretory lysosomes, exosomes, microvesicles, and autophagic vesicles, possibly through a mechanism similar to chaperone-mediated autophagy (CMA) (Andrei C et al. 2004; Ward JR et al. 2010; MacKenzie A et al. 2001; Gudipaty L et al. 2003; Qu Y et al. 2007; Iula L et al. 2018: reviewed by Eder C 2009; Piccioli P & Rubartelli A 2013; Claude-Taupin A et al. 2018). Further, the route of IL-1β secretion was found to be dependent on the type and strength of the inflammatory stimuli (Semino C et al. 2018; Sitia R & Rubartelli A 2018). Thus, in primary human monocytes small trauma or low pathogen load (LPS) activated a pathway involving secretory lysosomes that allows slow release of IL-1β, followed by apoptotic cell death that switches off the inflammatory response (Semino C et al. 2018). Differently, a stronger stimulus (LRZ) resulted in gasdermin D (GSDMD) cleavage with generation of the N-terminal domain that assembles in N-rings with formation of pores through which IL-1β can be externalized: this pathway of secretion is followed by pyroptosis, with membrane ruptures through which DAMPs can leave cells, further amplifying the inflammatory response (Semino C et al. 2018). Caspase-8 and FADD are required for NLRP3 inflammasome activation and IL-1β release (Gurung P et al. 2014, 2016). |
| (summation) | [BlackBoxEvent:449058] Interleukin-1 family are secreted [Homo sapiens] |
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