The Journal of Experimental Medicine
Torrey Pines Biolabs
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

Published online 5 February 2001.
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 380K)
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 Sabapathy, K.
Right arrow Articles by Wagner, E. F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sabapathy, K.
Right arrow Articles by Wagner, E. F.
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, 0022-1007/2001/2/317/ $5.00
The Journal of Experimental Medicine, Volume 193, Number 3, February 5, 2001 317-328


Original Article

C-Jun Nh2-Terminal Kinase (Jnk)1 and Jnk2 Have Similar and Stage-Dependent Roles in Regulating T Cell Apoptosis and Proliferation

Kanaga Sabapathya, Tuula Kallunkib, Jean-Pierre Davida, Isabella Graefc, Michael Karinb, and Erwin F. Wagnera

a Research Institute of Molecular Pathology, Vienna A 1030, Austria
b Department of Pharmacology, School of Medicine, Cancer Center, University of California at San Diego, La Jolla, California 92093
c Department of Pathology, Stanford Medical School, Stanford, California 94305
Research Institute of Molecular Pathology, Dr. Bohr-Gasse 7, Vienna A 1030, Austria.43-1-798-937043-1-797-30-888

wagner{at}nt.imp.univie.ac.at

Apoptotic and mitogenic stimuli activate c-Jun NH2-terminal kinases (JNKs) in T cells. Although T cells express both JNK1 and JNK2 isozymes, the absence of JNK2 alone can result in resistance to anti-CD3–induced thymocyte apoptosis and defective mature T cell proliferation. Similar defects in thymocyte apoptosis and mature T cell proliferation, the latter due to reduced interleukin 2 production, are also caused by JNK1 deficiency. Importantly, T cell function was compromised in Jnk1+/Jnk2+/ double heterozygous mice, indicating that JNK1 and JNK2 play similar roles in regulating T cell function. The reduced JNK dose results in defective c-Jun NH2-terminal phosphorylation in thymocytes but not in peripheral T cells, in which nuclear factors of activated T cells (NK-ATs)–DNA binding activity is affected. Thus, JNK1 and JNK2 control similar functions during T cell maturation through differential targeting of distinct substrates.

Key Words: apoptosis • JNK1 • JNK2 • proliferation • T lymphocyte


K. Sabapathy's present address is National Cancer Centre, Division of Cellular and Molecular Research, 11 Hospital Dr., Singapore 169610, Singapore. T. Kallunki's present address is Apoptosis Laboratory, Danish Cancer Society, Strandboulevarden 49, DK-2100, Copenhagen, Denmark.

Abbreviations used in this paper: dn, dominant negative; DP, double positive; ES, embryonic stem; GST, glutathione S-transferase; JNK, c-Jun NH2-terminal kinase; NF-ATc, cyclosporin A–sensitive NF-AT; NF-AT, nuclear factors of activated T cell.

© 2001 The Rockefeller University Press


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