Journal article
Interleukin-1 receptor-associated kinase 4 (IRAK4) plays a dual role in myddosome formation and Toll-like receptor signaling
D De Nardo, KR Balka, YC Gloria, VR Rao, E Latz, SL Masters
Journal of Biological Chemistry | AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC | Published : 2018
Open access
Abstract
Toll-like receptors (TLRs) form part of the host innate immune system, in which they act as sensors of microbial and endogenous danger signals. Upon TLR activation, the intracellular Toll/interleukin-1 receptor domains of TLR dimers initiate oligomerization of a multiprotein signaling platform comprising myeloid differentiation primary response 88 (MyD88) and members of the interleukin-1 receptor-associated kinase (IRAK) family. Formation of this myddosome complex initiates signal transduction pathways, leading to the activation of transcription factors and the production of inflammatory cytokines. To date, little is known about the assembly and disassembly of the myddosome and about the mec..
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Awarded by National Institutes of Health
Funding Acknowledgements
This work was funded in part by grant support from the BONFOR research commission (University of Bonn, Germany) (to D.D.N.); National Institutes of Health Grant 1R01AR066808-01A1, the Excellence Cluster Immuno-Sensation, and German Research Foundation Grants TRR83, 57, and SFB1123 (to E. L.); and NHMRC Grants 1144282, 1142354, and 1099262, the Sylvia and Charles Viertel Foundation, and an HHMI-Wellcome International Research Scholarship (to S. L. M.). V. R. is a paid employee of Pfizer Inc. E. L. is a co-founder and consultant to IFM Therapeutics. S. L. M. is a consultant to GlaxoSmithKline. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.