Weiss L, Whitmarsh A J, Yang D D, Rincón M, Davis R J, Flavell R A
Immunobiology Program, Department of Medicine, University of Vermont, Burlington, Vermont 05405, USA.
J Exp Med. 2000 Jan 3;191(1):139-46. doi: 10.1084/jem.191.1.139.
The c-Jun NH(2)-terminal kinases (JNKs) are a group of mitogen-activated protein (MAP) kinases that participate in signal transduction events mediating specific cellular functions. Activation of JNK is regulated by phosphorylation in response to cellular stress and inflammatory cytokines. Here, we demonstrate that JNK is regulated by a second, novel mechanism. Induction of Jnk gene expression is required in specific tissues before activation of this signaling pathway. The in vivo and in vitro ligation of the T cell receptor (TCR) leads to induction of JNK gene and protein expression. TCR signals are sufficient to induce JNK expression, whereas JNK phosphorylation also requires CD28-mediated costimulatory signals. Therefore, both expression and activation contribute to the regulation of the JNK pathway to ensure proper control during the course of an immune response.
c-Jun氨基末端激酶（JNKs）是一组丝裂原活化蛋白（MAP）激酶，参与介导特定细胞功能的信号转导事件。JNK的激活通过磷酸化来调节，以响应细胞应激和炎性细胞因子。在此，我们证明JNK受第二种新机制的调控。在该信号通路激活之前，特定组织中需要诱导Jnk基因表达。T细胞受体（TCR）的体内和体外连接导致JNK基因和蛋白表达的诱导。TCR信号足以诱导JNK表达，而JNK磷酸化也需要CD28介导的共刺激信号。因此，表达和激活都有助于JNK通路的调节，以确保在免疫反应过程中进行适当的控制。
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