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
Author:
Affiliation:
1. Institute of Biochemistry, University of Lausanne, BIL Biomedical Research Center, CH-1066 Epalinges, Switzerland
2. Department of Molecular Biology, Unit of Molecular Signal Transduction in Inflammation, Gent University, B-9000 Gent, Belgium
Abstract
Publisher
Rockefeller University Press
Subject
Immunology,Immunology and Allergy
Link
http://rupress.org/jem/article-pdf/197/2/263/1144448/jem1972263.pdf
Reference24 articles.
1. NF-κB Activation by Interleukin-1 (IL-1) Requires an IL-1 Receptor-associated Protein Kinase Activity
2. IRAK: A Kinase Associated with the Interleukin-1 Receptor
3. Interleukin (IL)-1 Receptor–associated Kinase (IRAK) Requirement for Optimal Induction of Multiple IL-1 Signaling Pathways and IL-6 Production
4. IL-1 Receptor-Associated Kinase Modulates Host Responsiveness to Endotoxin
5. IL-1-induced NF B and c-Jun N-terminal kinase (JNK) activation diverge at IL-1 receptor-associated kinase (IRAK)
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