|
||
Original Article |
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
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
![]()
CiteULike
Complore
Connotea
Del.icio.us
Digg
Facebook
Reddit
Technorati
Twitter What's this?
| TABLE OF CONTENTS |
|