This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Petersenn, S. Articles by Schulte, H. M. Search for Related Content PubMed PubMed Citation Articles by Petersenn, S. Articles by Schulte, H. M.

Identification of an Upstream Pituitary-Active Promoter of Human Somatostatin Receptor Subtype 5

IHF Institute for Hormone and Fertility Research, University of Hamburg (S.P., A.C.R., C.B.), 22529 Hamburg, Germany; Department of Medicine, University of Hamburg (S.P.), 20251 Hamburg, Germany; and Endokrinologikum Hamburg (H.M.S.), 22767 Hamburg, Germany

Address all correspondence and requests for reprints to: Dr. S. Petersenn, Division of Endocrinology, Medical Center, University of Essen, Hufelandstrasse 55, 45122 Essen, Germany. E-mail: . stephan.petersenn{at}uni-essen.de

Somatostatin receptor subtype 5 (sst5) has been linked to inhibition of PRL and insulin secretion. We characterized the genomic structure of the human sst5. The transcription start site was located 94 nucleotides upstream of the initiator ATG codon. Sequence analysis of 5'-inverse PCR products revealed the presence of a 6.1-kb intron in the 5'-untranslated region. RT-PCR analysis indicated tissue-specific activation of the newly identified upstream promoter in pituitary, but not in small intestine, lung, or placenta. A -1741 promoter directed significant levels of luciferase expression in GH₄ rat pituitary cells, Skut-1B endometrium cells, and JEG3 chorion carcinoma cells, which was absent in COS-7 monkey kidney cells. A minimal -101 promoter was sufficient to allow tissue-specific expression. Its activity in COS-7 cells was not enhanced by cotransfection of the pituitary-specific transcription factor Pit-1. Analysis of deletion constructs revealed a GC-rich region immediately upstream of the transcription start site, which is necessary for promoter activity. Somatostatin led to a significant inhibition, and forskolin and thyroid hormone to a significant stimulation of pituitary-specific promoter activity. Further mapping suggested a cAMP-responsive element located between -101 and the transcription start site, and thyroid hormone-responsive elements between -1741 and -1269 and between -317 and -101. These studies identified an upstream promoter of the sst5 gene with tissue-specific activity.

This article has been cited by other articles:

				C de Bruin, R A Feelders, A M Waaijers, P M van Koetsveld, D M Sprij-Mooij, S W J Lamberts, and L J Hofland Differential regulation of human dopamine D2 and somatostatin receptor subtype expression by glucocorticoids in vitro J. Mol. Endocrinol., January 1, 2009; 42(1): 47 - 56. [Abstract] [Full Text] [PDF]

				J. Torrisani, N. Hanoun, H. Laurell, F. Lopez, J.-J. Maoret, A. Souque, C. Susini, P. Cordelier, and L. Buscail Identification of an Upstream Promoter of the Human Somatostatin Receptor, hSSTR2, Which Is Controlled by Epigenetic Modifications Endocrinology, June 1, 2008; 149(6): 3137 - 3147. [Abstract] [Full Text] [PDF]

				G. Wang, X. Qi, W. Wei, E. W. Englander, and G. H. Greeley Jr. Characterization of the 5'-regulatory regions of the rat and human apelin genes and regulation of breast apelin by USF FASEB J, December 1, 2006; 20(14): 2639 - 2641. [Abstract] [Full Text] [PDF]