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• W26691815 abstract "Research Article1 November 1988free access Synergistic action of the glucocorticoid receptor with transcription factors. U. Strähle U. Strähle Institute of Cell and Tumor Biology, German Cancer Research Center, Heidelberg. Search for more papers by this author W. Schmid W. Schmid Institute of Cell and Tumor Biology, German Cancer Research Center, Heidelberg. Search for more papers by this author G. Schütz G. Schütz Institute of Cell and Tumor Biology, German Cancer Research Center, Heidelberg. Search for more papers by this author U. Strähle U. Strähle Institute of Cell and Tumor Biology, German Cancer Research Center, Heidelberg. Search for more papers by this author W. Schmid W. Schmid Institute of Cell and Tumor Biology, German Cancer Research Center, Heidelberg. Search for more papers by this author G. Schütz G. Schütz Institute of Cell and Tumor Biology, German Cancer Research Center, Heidelberg. Search for more papers by this author Author Information U. Strähle1, W. Schmid1 and G. Schütz1 1Institute of Cell and Tumor Biology, German Cancer Research Center, Heidelberg. The EMBO Journal (1988)7:3389-3395https://doi.org/10.1002/j.1460-2075.1988.tb03212.x PDFDownload PDF of article text and main figures. ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinked InMendeleyWechatReddit Figures & Info Steroid responsive elements (SRE) have been mapped at variable positions relative to the transcription start site and are often adjacent to binding sites of transcription regulatory proteins. In order to define the role of these transcriptional control sequences in the induction process, we inserted the previously defined 15-bp glucocorticoid response element (GRE) or 15-bp estrogen response element (ERE) immediately upstream of the TATA box of the thymidine kinase promoter, deleting all distal promoter elements. Both ERE and GRE confer inducibility by the respective hormone to the truncated promoter. These data suggest that the steroid receptor protein, possibly in conjunction with the TATA box binding protein, is able to form an active transcription complex. In contrast, the GRE when inserted 351 bp upstream of the start site of transcription of the tyrosine aminotransferase gene (TAT) is not capable of mediating hormone inducibility. Inducibility can be attained at this position by either two GREs or a single GRE in combination with a CCAAT motif. A cluster of point mutations in the CCAAT box abolishes hormone inducibility, strongly suggesting a synergistic action between the glucocorticoid receptor and the factor recognizing the CCAAT motif. The CCAAT box can be replaced by a CACCC box, an NF I and an SP1 binding site, thus demonstrating that synergistic action is not restricted to the CCAAT box binding protein. These combinations of a GRE with different transcription factor binding sites show a pronounced cell-type-dependent glucocorticoid induction of expression. Previous ArticleNext Article Volume 7Issue 111 November 1988In this issue RelatedDetailsLoading ..." @default.
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• W26691815 date "1988-11-01" @default.
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• W26691815 title "Synergistic action of the glucocorticoid receptor with transcription factors." @default.
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• W26691815 doi "https://doi.org/10.1002/j.1460-2075.1988.tb03212.x" @default.
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