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Details on Person Interleukin (IL)-1 signaling pathway is mediated by myeloid ...

Class:Id	Summation:5607977
_displayName	Interleukin (IL)-1 signaling pathway is mediated by myeloid ...
_timestamp	2014-07-16 02:05:04
created	[InstanceEdit:5607974] Shamovsky, Veronica, 2014-07-14
literatureReference	[LiteratureReference:5602701] Primary immunodeficiency to pneumococcal infection due to a defect in Toll-like receptor signaling [LiteratureReference:5602389] Pyogenic bacterial infections in humans with MyD88 deficiency [LiteratureReference:5602589] Functional assessment of the mutational effects of human IRAK4 and MyD88 genes [LiteratureReference:5602438] Natural loss-of-function mutation of myeloid differentiation protein 88 disrupts its ability to form Myddosomes [LiteratureReference:2428864] Two human MYD88 variants, S34Y and R98C, interfere with MyD88-IRAK4-myddosome assembly [LiteratureReference:5607905] MyD88 is an adaptor protein in the hToll/IL-1 receptor family signaling pathways [LiteratureReference:193914] MyD88, an adapter protein involved in interleukin-1 signaling [LiteratureReference:165864] IRAK-4 as the central TIR signaling mediator in innate immunity [LiteratureReference:936987] An oligomeric signaling platform formed by the Toll-like receptor signal transducers MyD88 and IRAK-4 [LiteratureReference:937049] Helical assembly in the MyD88-IRAK4-IRAK2 complex in TLR/IL-1R signalling [LiteratureReference:446653] Mass spectrometric analysis of the endogenous type I interleukin-1 (IL-1) receptor signaling complex formed after IL-1 binding identifies IL-1RAcP, MyD88, and IRAK-4 as the stable components
modified	[InstanceEdit:5609677] Shamovsky, Veronica, 2014-07-16
text	Interleukin (IL)-1 signaling pathway is mediated by myeloid differentiation primary response protein (MyD88), which interacts with interleukin-1 receptor(IL1R)-associated kinases (IRAKs) to form the Myddosome complex (MyD88:IRAK4:IRAK1/2) (Medzhitov R et al. 1998; Burns K et al. 1998; Suzuki N et al. 2002; Brikos C et al. 2007; Motshwene PG et al. 2009; Lin SC et al. 2010). The Myddosome transmits the signal leading to the activation of both nuclear factor ?B (NF?B) and mitogen-acivator protein kinases (MAPKs). Autosomal recessive MyD88 deficiency predispose affected patients to recurrent pyogenic bacterial infection due to abolished IL1R-mediated cytokine responses of the blood cells (von Bernuth H et al. 2008; Currie AJ et al. 2004). Here we describe several natural loss-of-function MyD88 variants (E52del, L93P, E65del, S34T) that showed severely reduced NF?B activation in human cell-based assays due to either reduced homooligomerization or impaired interaction with IRAK4, the two crucial events in the assembly of the Myddosome complex (George J et al. 2011; Nagpal K et al. 2011; Yamamoto T et al. 2014).
(summation)	[Pathway:5602586] MyD88 deficiency (IL1R) [Homo sapiens]
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