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Details on Person All TLRs, except for TLR3, employ the MyD88-dependent signal...

Class:Id	Summation:5607803
_displayName	All TLRs, except for TLR3, employ the MyD88-dependent signal...
_timestamp	2014-10-06 04:30:55
created	[InstanceEdit:5607794] 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
modified	[InstanceEdit:5625553] Shamovsky, Veronica, 2014-10-06
text	All TLRs, except for TLR3, employ the MyD88-dependent signaling pathway. Autosomal recessive MyD88 deficiency predispose affected patients to recurrent pyogenic bacterial infection due to abolished TLR-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 NFkB activation in human cell-based assays due to reduced homooligomerization and IRAK4 interaction, 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)	[FailedReaction:5602383] Defective MyD88 does not oligomerize within the activated TLR2/4 complex [Homo sapiens]
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