The Journal of Experimental Medicine
VeriKine-HS Human IFN-Beta
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 227K)
Right arrow PPT slides of all figures
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JEM
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Muzio, M.
Right arrow Articles by Mantovani, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Muzio, M.
Right arrow Articles by Mantovani, A.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Facebook   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?
© The Rockefeller University Press, 0022-1007/1998/6/2097/ $5.00
The Journal of Experimental Medicine, Volume 187, Number 12, June 15, 1998 2097-2101

Brief Definitive Reports

The Human Toll Signaling Pathway: Divergence of Nuclear Factor {kappa}B and JNK/SAPK Activation Upstream of Tumor Necrosis Factor Receptor–associated Factor 6 (TRAF6)

Marta Muzio*, Gioacchino Natoli{ddagger}, Simona Saccani*, Massimo Levrero{ddagger}, and Alberto Mantovani*,§

From the * Department of Immunology and Cell Biology, Mario Negri Institute, I-20157 Milan, Italy; {ddagger} Istituto di I Clinica Medica, Policlinico Umberto I, I-00161 Rome, Italy; and § Department of Biotechnology, University of Brescia, 25123 Brescia, Italy

The human homologue of Drosophila Toll (hToll) is a recently cloned receptor of the interleukin 1 receptor (IL-1R) superfamily, and has been implicated in the activation of adaptive immunity. Signaling by hToll is shown to occur through sequential recruitment of the adapter molecule MyD88 and the IL-1R–associated kinase. Tumor necrosis factor receptor–activated factor 6 (TRAF6) and the nuclear factor {kappa}B (NF-{kappa}B)–inducing kinase (NIK) are both involved in subsequent steps of NF-{kappa}B activation. Conversely, a dominant negative version of TRAF6 failed to block hToll-induced activation of stress-activated protein kinase/c-Jun NH2-terminal kinases, thus suggesting an early divergence of the two pathways.

Key Words: Toll • interleukin 1 receptor • nuclear factor {kappa}B • c-Jun NH2-terminal kinase/ stress-activated protein kinase

Address correspondence to Marta Muzio, Dept. Immunology and Cell Biology, Mario Negri Institute, via Eritrea 62, I-20157, Milano, Italy. Phone: 39-2-39014532; Fax: 39-2-3546277; E-mail: muziom{at}irfmn.mnegri.it

M. Muzio is supported by Federazione Italiana Ricerca sul Cancro. This work was supported by European Community Special Project Biotechnology, Consiglio Nazionale Ricerche, and Associazione Italiana Ricerca sul Cancro.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Facebook Facebook   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?




  Home | Help | Feedback | Subscriptions | Archive | Search
TABLE OF CONTENTS