The estrogen-responsive element as an inducible enhancer: DNA sequence requirements and conversion to a glucocorticoid-responsive element.

Détails

ID Serval
serval:BIB_C4F221A04EB4
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
The estrogen-responsive element as an inducible enhancer: DNA sequence requirements and conversion to a glucocorticoid-responsive element.
Périodique
EMBO Journal
Auteur(s)
Martinez E., Givel F., Wahli W.
ISSN
0261-4189[print], 0261-4189[linking]
Statut éditorial
Publié
Date de publication
12/1987
Volume
6
Numéro
12
Pages
3719-3727
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
The estrogen-responsive element (ERE) present in the 5'-flanking region of the Xenopus laevis vitellogenin (vit) gene B1 has been characterized by transient expression analysis of chimeric vit-tk-CAT (chloramphenicol acetyltransferase) gene constructs transfected into the human estrogen-responsive MCF-7 cell line. The vit B1 ERE behaves like an inducible enhancer, since it is able to confer estrogen inducibility to the heterologous HSV thymidine kinase (tk) promoter in a relative position- and orientation-independent manner. In this assay, the minimal B1 ERE is 33 bp long and consists of two 13 bp imperfect palindromic elements both of which are required for the enhancer activity. A third imperfect palindromic element is present further upstream within the 5'-flanking region of the gene but is unable to confer hormone responsiveness by itself. Similarly, neither element forming the B1 ERE can alone confer estrogen inducibility to the tk promoter. However, in combinations of two, all three imperfect palindromes can act cooperatively to form a functional ERE. In contrast a single 13 bp perfect palindromic element, GGTCACTGTGACC, such as the one found upstream of the vit gene A2, is itself sufficient to act as a fully active ERE. Single point mutations within this element abolish estrogen inducibility, while a defined combination of two mutations converts this ERE into a glucocorticoid-responsive element.
Mots-clé
Acetyltransferases/genetics, Animals, Base Sequence, Cell Line, Chimera, Chloramphenicol O-Acetyltransferase, Chromosome Deletion, Dexamethasone/pharmacology, Enhancer Elements, Genetic/drug effects, Estradiol/pharmacology, Female, Genes, Molecular Sequence Data, Mutation, Transcription, Genetic, Transfection, Vitellogenins/genetics, Xenopus laevis
Pubmed
Web of science
Création de la notice
24/01/2008 17:05
Dernière modification de la notice
03/03/2018 21:14
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