HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Wietek, C. Articles by O’Neill, L. A. Search for Related Content PubMed PubMed Citation Articles by Wietek, C. Articles by O’Neill, L. A.

IRAK-4: A New Drug Target in Inflammation, Sepsis, and Autoimmunity

Department of Biochemistry, Trinity College, Dublin 2, Ireland

SUMMARY

Two very recent publications, by Suzuki et al. and Li et al., describe the cloning, characterization, and the effects of knockout mice deficient in interleukin-1-associated receptor kinase-4 (IRAK-4), the newest member of the IRAK family. IRAK-4 requires its kinase activity to activate NF-B, and IRAK-4 also activates MAP kinases. Wietek and O’Neill discuss the data indicating that IRAK-4 lies upstream of and activates IRAK-1, and that IRAK-4 is essential for innate immunity.

This article has been cited by other articles:

				A. Kuglstatter, A. G. Villasenor, D. Shaw, S. W. Lee, S. Tsing, L. Niu, K. W. Song, J. W. Barnett, and M. F. Browner Cutting Edge: IL-1 Receptor-Associated Kinase 4 Structures Reveal Novel Features and Multiple Conformations J. Immunol., March 1, 2007; 178(5): 2641 - 2645. [Abstract] [Full Text] [PDF]

				M. V. Lasker, M. M. Gajjar, and S. K. Nair Cutting Edge: Molecular Structure of the IL-1R-Associated Kinase-4 Death Domain and Its Implications for TLR Signaling J. Immunol., October 1, 2005; 175(7): 4175 - 4179. [Abstract] [Full Text] [PDF]