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Article: Functional mapping of a placenta-specific upstream promoter for human gonadotropin-releasing hormone receptor gene

TitleFunctional mapping of a placenta-specific upstream promoter for human gonadotropin-releasing hormone receptor gene
Authors
Issue Date2001
PublisherThe Endocrine Society. The Journal's web site is located at http://endo.endojournals.org
Citation
Endocrinology, 2001, v. 142 n. 4, p. 1506-1516 How to Cite?
AbstractGnRH has been showed to regulate hCG expression and secretion from the placenta through a GnRH receptor (GnRHR)-mediated process. Recently, we have reported the isolation of human GnRHR full-length complementary DNA from the human placental cells including choriocarcinoma JEG-3 cells, immortalized extravillous trophoblasts, and primary cultures of trophoblasts. Despite these observations, the molecular mechanism that controls the transcription regulation of the GnRHR gene expression in the placenta remains unknown. Here we described the identification of an upstream placenta-specific promoter located between nucleotide (nt) -1737 and -1346 (relative to the translation start site) for the human GnRHR gene. Using transient transfection studies, this upstream promoter has been shown to determine the placental cell-specific expression of this gene. Primer extension studies further confirmed the utilization of this promoter in JEG-3 cells in vivo. By mutagenesis coupled to functional studies, we have identified four putative transcription factor-binding sites, namely human glucocorticoid receptor (hGR)-Oct-1 (nt -1718 to -1710), hGR-cAMP response element (CRE; nt -1649 to -1641), hGR-GATA (nt -1602 to -1597), and hGR-activating protein-1 (nt -1518 to -1511), that are essential to the expression of this gene. Mutations of these cis-acting motifs reduced the promoter activity. The CRE and GATA motifs were subsequently shown to be placenta specific, as mutations of these motifs caused a dramatic loss in promoter activities in the placental JEG-3 cells, but not in the ovarian carcinoma OVCAR-3, monkey kidney COS-1, and human embryonic kidney 293 cells. Gel mobility assays confirmed the binding of nuclear proteins Oct-1, CRE-binding protein, GATA-2, GATA-3, c-Fos, and c-Jun from JEG-3 cells to these four elements.
Persistent Identifierhttp://hdl.handle.net/10722/84676
ISSN
2015 Impact Factor: 4.159
2015 SCImago Journal Rankings: 2.363
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorKwai Wa Chengen_HK
dc.contributor.authorChow, BKCen_HK
dc.contributor.authorLeung, PCKen_HK
dc.date.accessioned2010-09-06T08:55:49Z-
dc.date.available2010-09-06T08:55:49Z-
dc.date.issued2001en_HK
dc.identifier.citationEndocrinology, 2001, v. 142 n. 4, p. 1506-1516en_HK
dc.identifier.issn0013-7227en_HK
dc.identifier.urihttp://hdl.handle.net/10722/84676-
dc.description.abstractGnRH has been showed to regulate hCG expression and secretion from the placenta through a GnRH receptor (GnRHR)-mediated process. Recently, we have reported the isolation of human GnRHR full-length complementary DNA from the human placental cells including choriocarcinoma JEG-3 cells, immortalized extravillous trophoblasts, and primary cultures of trophoblasts. Despite these observations, the molecular mechanism that controls the transcription regulation of the GnRHR gene expression in the placenta remains unknown. Here we described the identification of an upstream placenta-specific promoter located between nucleotide (nt) -1737 and -1346 (relative to the translation start site) for the human GnRHR gene. Using transient transfection studies, this upstream promoter has been shown to determine the placental cell-specific expression of this gene. Primer extension studies further confirmed the utilization of this promoter in JEG-3 cells in vivo. By mutagenesis coupled to functional studies, we have identified four putative transcription factor-binding sites, namely human glucocorticoid receptor (hGR)-Oct-1 (nt -1718 to -1710), hGR-cAMP response element (CRE; nt -1649 to -1641), hGR-GATA (nt -1602 to -1597), and hGR-activating protein-1 (nt -1518 to -1511), that are essential to the expression of this gene. Mutations of these cis-acting motifs reduced the promoter activity. The CRE and GATA motifs were subsequently shown to be placenta specific, as mutations of these motifs caused a dramatic loss in promoter activities in the placental JEG-3 cells, but not in the ovarian carcinoma OVCAR-3, monkey kidney COS-1, and human embryonic kidney 293 cells. Gel mobility assays confirmed the binding of nuclear proteins Oct-1, CRE-binding protein, GATA-2, GATA-3, c-Fos, and c-Jun from JEG-3 cells to these four elements.en_HK
dc.languageengen_HK
dc.publisherThe Endocrine Society. The Journal's web site is located at http://endo.endojournals.orgen_HK
dc.relation.ispartofEndocrinologyen_HK
dc.rightsEndocrinology. Copyright © The Endocrine Society.en_HK
dc.titleFunctional mapping of a placenta-specific upstream promoter for human gonadotropin-releasing hormone receptor geneen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0013-7227&volume=142&spage=1506&epage=1516&date=2001&atitle=Functional+Mapping+of+a+Placenta-Specific+Upstream+Promoter+for+Human+Gonadotropin-Releasing+Hormone+Receptor+Geneen_HK
dc.identifier.emailChow, BKC: bkcc@hku.hken_HK
dc.identifier.authorityChow, BKC=rp00681en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1210/en.142.4.1506en_HK
dc.identifier.pmid11250931-
dc.identifier.scopuseid_2-s2.0-0035053010en_HK
dc.identifier.hkuros56627en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035053010&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume142en_HK
dc.identifier.issue4en_HK
dc.identifier.spage1506en_HK
dc.identifier.epage1516en_HK
dc.identifier.isiWOS:000167845900018-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridKwai Wa Cheng=7409533824en_HK
dc.identifier.scopusauthoridChow, BKC=7102826193en_HK
dc.identifier.scopusauthoridLeung, PCK=55419381000en_HK

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