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Details on Person The MyD88 adaptor protein links ligand-bound TLR7 and TLR8 t...
| Class:Id | Summation:5607955 |
|---|---|
| _displayName | The MyD88 adaptor protein links ligand-bound TLR7 and TLR8 t... |
| _timestamp | 2018-10-31 22:49:16 |
| created | [InstanceEdit:5607968] 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:9627051] Shamovsky, Veronica, 2018-10-31 |
| text | The MyD88 adaptor protein links ligand-bound TLR7 and TLR8 to IRAK kinases by assembling the Myddosome complex. 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 NF-kappa B 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:5602393] Defective MyD88 does not oligomerize within the activated TLR7/8 complex [Homo sapiens] |
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