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Article: Oct-1 is involved in the transcriptional repression of the gonadotropin-releasing hormone receptor gene

TitleOct-1 is involved in the transcriptional repression of the gonadotropin-releasing hormone receptor gene
Authors
Issue Date2002
PublisherThe Endocrine Society. The Journal's web site is located at http://endo.endojournals.org
Citation
Endocrinology, 2002, v. 143 n. 12, p. 4693-4701 How to Cite?
AbstractPrevious deletion analysis of the 5′-flanking region of human GnRH receptor (GnRHR) gene has revealed a powerful negative regulatory element (NRE) located between nucleotide -1017 and -771. In the present study, we demonstrated that this NRE could repress the homologous promoter, irrespective of its position and completely abolish the activity of a heterologous thymidine kinase promoter in an orientation-dependent manner. Progressive 3′-deletion analysis revealed that most of the silencing activity of the NRE resided in a putative octamer regulatory sequence (5′AAGCAAACT3′), which alone could repress the promoter activities by 69-90% in ovarian OVCAR-3, placental JEG-3, and gonadotropederived αT3-1 cells. Mutation of the AAAC residues of the octamer sequence completely removed its silencing activity. Interestingly, conversion of the octamer sequence into that of the rodent GnRHR promoter (5′AAGCAAAGT3′) did not attenuate its silencing effect, indicating that the repressive role of the octamer sequence is evolutionarily conserved. EMSAs showed that common DNA-protein complexes of the same mobility were formed with nuclear extracts from the reproductive cells and gonadotropes, and a consensus octamer transcription factor-1 (Oct-1) binding sequence could dose dependently inhibit the complex formation. Antibody supershift and Southwestern blot assays confirmed that the protein binding to the octamer sequence was the ubiquitously expressed transcription factor Oct-1. Overexpression of Oct-1 augmented the silencing activity of the octamer sequence in αT3-1 cells. Taken together, our results clearly indicate a role of Oct-1 in the transcriptional repression of the human GnRHR gene.
Persistent Identifierhttp://hdl.handle.net/10722/84953
ISSN
2015 Impact Factor: 4.159
2015 SCImago Journal Rankings: 2.363
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheng, CKen_HK
dc.contributor.authorYeung, CMen_HK
dc.contributor.authorHoo, RLCen_HK
dc.contributor.authorChow, BKCen_HK
dc.contributor.authorLeung, PCKen_HK
dc.date.accessioned2010-09-06T08:59:02Z-
dc.date.available2010-09-06T08:59:02Z-
dc.date.issued2002en_HK
dc.identifier.citationEndocrinology, 2002, v. 143 n. 12, p. 4693-4701en_HK
dc.identifier.issn0013-7227en_HK
dc.identifier.urihttp://hdl.handle.net/10722/84953-
dc.description.abstractPrevious deletion analysis of the 5′-flanking region of human GnRH receptor (GnRHR) gene has revealed a powerful negative regulatory element (NRE) located between nucleotide -1017 and -771. In the present study, we demonstrated that this NRE could repress the homologous promoter, irrespective of its position and completely abolish the activity of a heterologous thymidine kinase promoter in an orientation-dependent manner. Progressive 3′-deletion analysis revealed that most of the silencing activity of the NRE resided in a putative octamer regulatory sequence (5′AAGCAAACT3′), which alone could repress the promoter activities by 69-90% in ovarian OVCAR-3, placental JEG-3, and gonadotropederived αT3-1 cells. Mutation of the AAAC residues of the octamer sequence completely removed its silencing activity. Interestingly, conversion of the octamer sequence into that of the rodent GnRHR promoter (5′AAGCAAAGT3′) did not attenuate its silencing effect, indicating that the repressive role of the octamer sequence is evolutionarily conserved. EMSAs showed that common DNA-protein complexes of the same mobility were formed with nuclear extracts from the reproductive cells and gonadotropes, and a consensus octamer transcription factor-1 (Oct-1) binding sequence could dose dependently inhibit the complex formation. Antibody supershift and Southwestern blot assays confirmed that the protein binding to the octamer sequence was the ubiquitously expressed transcription factor Oct-1. Overexpression of Oct-1 augmented the silencing activity of the octamer sequence in αT3-1 cells. Taken together, our results clearly indicate a role of Oct-1 in the transcriptional repression of the human GnRHR gene.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.-
dc.subject.meshBinding Sites-
dc.subject.meshDNA-Binding Proteins - chemistry - genetics - physiology-
dc.subject.meshReceptors, LHRH - genetics-
dc.subject.meshRepressor Proteins - physiology-
dc.subject.meshTranscription Factors - chemistry - genetics - physiology-
dc.titleOct-1 is involved in the transcriptional repression of the gonadotropin-releasing hormone receptor geneen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0013-7227&volume=143&issue=12&spage=4693&epage=4701&date=2002&atitle=Oct-1+Is+Involved+in+the+Transcriptional+Repression+of+the+Gonadotropin-Releasing+Hormone+Receptor+Geneen_HK
dc.identifier.emailHoo, RLC:rubyhoo@hkucc.hku.hken_HK
dc.identifier.emailChow, BKC:bkcc@hku.hken_HK
dc.identifier.authorityHoo, RLC=rp01334en_HK
dc.identifier.authorityChow, BKC=rp00681en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1210/en.2002-220576en_HK
dc.identifier.pmid12446597-
dc.identifier.scopuseid_2-s2.0-0036893336en_HK
dc.identifier.hkuros85713en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036893336&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume143en_HK
dc.identifier.issue12en_HK
dc.identifier.spage4693en_HK
dc.identifier.epage4701en_HK
dc.identifier.isiWOS:000179543900025-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridCheng, CK=7404797040en_HK
dc.identifier.scopusauthoridYeung, CM=7201354151en_HK
dc.identifier.scopusauthoridHoo, RLC=6602369766en_HK
dc.identifier.scopusauthoridChow, BKC=7102826193en_HK
dc.identifier.scopusauthoridLeung, PCK=7401747829en_HK

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