|
|
|
|
|
|
|
||
Address correspondence to Laurie H. Glimcher at her present address, Dept. of Medicine, Harvard Medical School, Boston, MA 02115. Phone: (617) 432-0622; Fax: (617) 432-0084; email: lglimche{at}hsph.harvard.edu
The activator protein 1 (AP-1) transcription factor is a key participant in the control of T cell proliferation, cytokine production, and effector function. In the immune system, AP-1 activity is highest in T cells, suggesting that a subset of T cell–specific coactivator proteins exist to selectively potentiate AP-1 function. Here, we describe that the expression of Schnurri-3, also known as
recognition component (KRC), is induced upon T cell receptor signaling in T cells and functions to regulate the expression of the interleukin 2 (IL-2) gene. Overexpression of KRC in transformed and primary T cells leads to increased IL-2 production, whereas dominant-negative KRC, or loss of KRC protein in KRC-null mice, results in diminished IL-2 production. KRC physically associates with the c-Jun transcription factor and serves as a coactivator to augment AP-1–dependent IL-2 gene transcription.
Key Words: ZAS domain • coactivator • cytokines • AP-1 • TCR signaling
Abbreviations used in this paper:
-NAC, chain of the nascent polypeptide-associated complex; AP-1, activator protein 1; CBP, CREB-binding protein; ERK, extracellular regulated kinase; JAB-1, Jun-activating binding protein 1; JNK, c-Jun NH2-terminal kinase; KRC, recognition component; MAPK, mitogen-activated protein kinase; NF, nuclear factor; Rss, recombination signal sequence; SEE, staphylococcus enterotoxin E; ZAS, zinc finger acidic domain structure.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Facebook 
Reddit 
Technorati 
Twitter What's this?
This article has been cited by other articles:
| TABLE OF CONTENTS |
|
