Expression of immediate early gene pip92 during anisomycin-induced cell death is mediated by the JNK- and p38-dependent activation of Elk1

被引:38
作者
Chung, KC
Kim, SM
Rhang, SG
Lau, LF
Gomes, I
Ahn, YS
机构
[1] Yonsei Univ, Coll Med, Dept Pharmacol, Seoul 120752, South Korea
[2] Yonsei Univ, Coll Med, Brain Res Inst, Seoul 120752, South Korea
[3] Hongik Univ, Sci & Technol Res Inst, Seoul, South Korea
[4] Univ Illinois, Coll Med, Dept Genet, Chicago, IL 60612 USA
[5] Univ Chicago, Ben May Inst Canc Res, Chicago, IL 60637 USA
[6] Univ Chicago, Dept Pharmacol & Physiol Sci, Chicago, IL 60637 USA
来源
EUROPEAN JOURNAL OF BIOCHEMISTRY | 2000年 / 267卷 / 15期
关键词
pip92; anisomycin; cell death; MAP kinase; Elk1;
D O I
10.1046/j.1432-1327.2000.01517.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
We report here that immediate early gene pip92 is expressed during anisomycin-induced cell death in fibroblast NIH3T3 cells. To determine the mechanism by which this occurs and to identify downstream signaling pathways, we investigated the induction of the pip92 promoter. The activation of pip92 by anisomycin is mediated by the activation of MAP kinases, such as JNK and p38 kinase, but not ERK. Deletion analysis of the pip92 promoter indicated that pip92 activation occurs primarily within the region containing a serum response element (SRE). Further analysis of the SRE using a heterologous thymidine kinase promoter showed that both an Ets and CArG-like site are required for anisomycin-induced pip92 expression. Elk1, which binds to the Ets site, was phosphorylated by the JNK- and p38-dependent pathways and the phosphorylation of Elk1-GAL4 fusion proteins by these pathways was sufficient for the transactivation. Overall, this study suggested that different MAPK pathways are involved in the expression of immediate early gene pip92 by growth factors and environmental stresses.
引用
收藏
页码:4676 / 4684
页数:9
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