Transcriptional activation of the Egr-1 gene mediated by tetradecanoylphorbol acetate and extracellular signal-regulated protein kinase

被引：29

作者：

Bauer, I

Hohl, M

Al-Sarraj, A

Vinson, C

Thiel, G ^{[1
]}

机构：

[1] Univ Saarland, Ctr Med, Dept Med Biochem & Mol Biol, D-66421 Homburg, Germany

[2] Univ Saarland, Ctr Med, Dept Anesthesiol & Crit Care Med, D-66421 Homburg, Germany

[3] NCI, NIH, Lab Metab, Bethesda, MD 20892 USA

来源：

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS | 2005年 / 438卷 / 01期

关键词：

CRE; CREB; Egr-1; Elk-1; MAP kinase phosphatase 1; phorbol ester; serum response element; transcription;

D O I：

10.1016/j.abb.2005.03.016

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：

Activation of extracellular signal-regulated protein kinase (ERK) triggers the biosynthesis of Egr-1, a zinc finger transcription factor. Likewise, the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) strongly upregulates Egr-1 biosynthesis. Here, we have analyzed the genetic elements involved in the regulation of Egr-1 gene transcription by ERK and TPA in human hepatoma cells. Expression experiments using mitogen-activated protein kinase phosphatase-1 or a dominant-negative mutant of the ternary complex factor Elk-1 revealed that the distal cluster of serum response elements is essential in the TPA-induced enhancement of Egr-1 promoter activity, encompassing two independent TPA-responsive elements. The CRE in the proximal Egr-1 promoter plays, if anything, only a marginal role in TPA-induced stimulus-transcription coupling of the Egr-1 gene. The fact that Egr-1 promoter/reporter gene transcription is upregulated by a constitutively active CREB mutant indicates that the CRE couples other signaling cascades via CREB to the Egr-1 gene. (c) 2005 Elsevier Inc. All rights reserved.

引用

页码：36 / 52

页数：17

共 55 条

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