The DOI matches its Crossref record; 24 of the 24 references it cites were found in a registry or an index.
Inhibition of Interleukin 1 Receptor/Toll-like Receptor Signaling through the Alternatively Spliced, Short Form of MyD88 Is Due to Its Failure to Recruit IRAK-4
Open accessAbstract
Toll-like receptors (TLRs) and members of the proinflammatory interleukin 1 receptor (IL-1R) family are dependent on the presence of MyD88 for efficient signal transduction. The bipartite nature of MyD88 (N-terminal death domain [DD] and COOH-terminal Toll/IL-1 receptor [TIR] domain) allows it to link the TIR domain of IL-1R/TLR with the DD of the Ser/Thr kinase termed IL-1R–associated kinase (IRAK)-1. This triggers IRAK-1 phosphorylation and in turn the activation of multiple signaling cascades such as activation of the transcription factor nuclear factor (NF)-κB. In contrast, expression of MyD88 short (MyD88s), an alternatively spliced form of MyD88 that lacks only the short intermediate domain separating the DD and TIR domains, leads to a shutdown of IL-1/lipopolysaccharide-induced NF-κB activation. Here, we provide the molecular explanation for this difference. MyD88 but not MyD88s strongly interacts with IRAK-4, a newly identified kinase essential for IL-1R/TLR signaling. In the presence of MyD88s, IRAK-1 is not phosphorylated and neither activates NF-κB nor is ubiquitinated. Thus, MyD88s acts as a negative regulator of IL-1R/TLR/MyD88-triggered signals, leading to a transcriptionally controlled negative regulation of innate immune responses.
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Cites
Unresponsiveness of MyD88-Deficient Mice to Endotoxin
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Targeted Disruption of the MyD88 Gene Results in Loss of IL-1- and IL-18-Mediated Function
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TRAF6 is a signal transducer for interleukin-1
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IRAK-M Is a Negative Regulator of Toll-like Receptor Signaling
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IRAK (Pelle) Family Member IRAK-2 and MyD88 as Proximal Mediators of IL-1 Signaling
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Severe impairment of interleukin-1 and Toll-like receptor signalling in mice lacking IRAK-4
Suzuki, N., Suzuki, S., Duncan, G. S., Millar, D. G., Wada, T., Mirtsos, C., Takada, H., Wakeham, A., Itie, A., Li, S., et al. (2002) · Nature · doi:10.1038/nature736 · Cited by 853
IRAK-4: A novel member of the IRAK family with the properties of an IRAK-kinase
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MyD88, an Adapter Protein Involved in Interleukin-1 Signaling
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Self-citation
Cited by
Akira, S., & Takeda, K. (2004) · Nature reviews. Immunology · doi:10.1038/nri1391 · Cited by 8,312
Hayden, M. S., & Ghosh, S. (2004) · Genes & Development · doi:10.1101/gad.1228704 · Cited by 3,842
LPS/TLR4 signal transduction pathway
Lu, Y.-C., Yeh, W.-C., & Ohashi, P. S. (2008) · Cytokine · doi:10.1016/j.cyto.2008.01.006 · Cited by 3,301
Toll-like receptors in innate immunity
Takeda, K. (2004) · International Immunology · doi:10.1093/intimm/dxh186 · Cited by 3,328
Pathogen Recognition and Inflammatory Signaling in Innate Immune Defenses
Mogensen, T. H. (2009) · Clinical Microbiology Reviews · doi:10.1128/cmr.00046-08 · Cited by 3,111
Metadata
- Authors
- Burns, K., Janssens, S., Brissoni, B., Olivos, N., Beyaert, R., & Tschopp, J.
- Venue
- The Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2003-01-13
- Volume
- 197
- Issue
- 2
- Pages
- 263-268
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- OpenAlex
- W2145110660
- Cited by
- 512
- References
- 24
- FWCI
- 10.61
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Burns, K., Janssens, S., Brissoni, B., Olivos, N., Beyaert, R., & Tschopp, J. (2003). Inhibition of Interleukin 1 Receptor/Toll-like Receptor Signaling through the Alternatively Spliced, Short Form of MyD88 Is Due to Its Failure to Recruit IRAK-4. The Journal of Experimental Medicine. https://doi.org/10.1084/jem.20021790
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