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dc.contributor.authorAlotaibi, H.en_US
dc.contributor.authorYaman, E. C.en_US
dc.contributor.authorDemirpence, E.en_US
dc.contributor.authorTazebay, U. H.en_US
dc.date.accessioned2015-07-28T11:57:56Z
dc.date.available2015-07-28T11:57:56Z
dc.date.issued2006en_US
dc.identifier.issn0006-291X
dc.identifier.urihttp://hdl.handle.net/11693/11504
dc.description.abstractThe function of sodium iodide symporter (Na+/I symporter, or NIS) in mammary epithelial cells is essential for the accumulation of I in milk; the newborn’s first source of I for thyroid hormone synthesis. Furthermore, increased mammary gland NIS expression has previously been shown in human breast cancer. Several hormones and factors including all-trans-retinoic acid (tRA) regulate the expression of NIS. In this study, using breast cancer cell lines, we established that tRA-responsive NIS expression is confined to estrogen receptor- a (ERa) positive cells and we investigated the role of ERa in the regulation of NIS expression. We showed that the suppression of endogenous ERa by RNA interference downregulates NIS expression in ERa positive mammary cells. Besides, in an ERa negative cell line, reintroduction of ERa resulted in the expression of NIS in a ligand-independent manner. We also identified a novel estrogen-responsive element in the promoter region of NIS that specifically binds ERa and mediates ERa-dependent activation of transcription. Our results indicate that unliganded ERa (apo-ERa) contributes to the regulation of NIS gene expression. 2006 Elsevier Inc. All rights reserved.en_US
dc.language.isoEnglishen_US
dc.source.titleBiochemical and Biophysical Research Communicationsen_US
dc.relation.isversionofhttp://dx.doi.org/10.1016/j.bbrc.2006.05.049en_US
dc.subjectIodide Transporten_US
dc.subjectNisen_US
dc.subjectEstrogen Receptoren_US
dc.subjectMammary Glanden_US
dc.subjectBreast Canceren_US
dc.titleUnliganded estrogen receptor-x activates transcription of the mammary gland Na+/I-symporter geneen_US
dc.typeArticleen_US
dc.departmentDepartment of Molecular Biology and Geneticsen_US
dc.citation.spage1487en_US
dc.citation.epage1496en_US
dc.citation.volumeNumber345en_US
dc.citation.issueNumber4en_US
dc.identifier.doi10.1016/j.bbrc.2006.05.049en_US
dc.publisherElsevieren_US


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