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Regulation of life and death by the zinc finger transcription factor Egr‐1

Identifieur interne : 000C40 ( Istex/Curation ); précédent : 000C39; suivant : 000C41

Regulation of life and death by the zinc finger transcription factor Egr‐1

Auteurs : Gerald Thiel [Allemagne] ; Giuseppe Cibelli [Allemagne, Italie]

Source :

RBID : ISTEX:7C70296D46BCF99982A0B16531F96FC199885AC8

English descriptors

Abstract

The biosynthesis of the zinc finger transcription factor Egr‐1 is stimulated by many extracellular signaling molecules including hormones, neurotransmitters, growth and differentiation factors, and cytotoxic metabolites. The 5′‐flanking region of the Egr‐1 gene contains genetic elements that are essential in connecting stimulation of the cells with enhanced transcription of the Egr‐1 gene, and subsequently, transcription of Egr‐1‐responsive genes. Thus, Egr‐1 links cellular signaling cascades with changes in the gene expression pattern. Many biological functions have been attributed to Egr‐1. Here, we discuss evidence for Egr‐1 control of cellular proliferation and programmed cell death. J. Cell. Physiol. 193: 287–292, 2002. © 2002 Wiley‐Liss, Inc.

Url:
DOI: 10.1002/jcp.10178

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ISTEX:7C70296D46BCF99982A0B16531F96FC199885AC8

Le document en format XML

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<div type="abstract" xml:lang="en">The biosynthesis of the zinc finger transcription factor Egr‐1 is stimulated by many extracellular signaling molecules including hormones, neurotransmitters, growth and differentiation factors, and cytotoxic metabolites. The 5′‐flanking region of the Egr‐1 gene contains genetic elements that are essential in connecting stimulation of the cells with enhanced transcription of the Egr‐1 gene, and subsequently, transcription of Egr‐1‐responsive genes. Thus, Egr‐1 links cellular signaling cascades with changes in the gene expression pattern. Many biological functions have been attributed to Egr‐1. Here, we discuss evidence for Egr‐1 control of cellular proliferation and programmed cell death. J. Cell. Physiol. 193: 287–292, 2002. © 2002 Wiley‐Liss, Inc.</div>
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