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pubmed-article:12590942pubmed:abstractTextNeuropeptide Y (NPY) plays an important role in the central and sympathetic regulation of food intake and blood pressure. Although the NPY gene expression is regulated by a number of agents such as leptin, the mechanism responsible for leptin-induced regulation of the transcription of the NPY gene remains to be explored. In this study, the NPY gene promoter was transactivated by leptin in N18TG2, NG108-15 and PC12 cells which expressed the functional leptin receptor. The long isoform of leptin receptor (OB-Rb) could induce the transactivation, but the C-terminal truncated form (OB-Ra) could not. When dominant negative type of STAT3, JAK1 or JAK2 and was co-expressed, the leptin-induced transactivation was suppressed almost completely. The leptin-response element which confers NPY gene transactivation by leptin was determined in the 221-bp region of rat NPY gene promoter (-553/-335), where two STAT3-binding site-like elements (TCCAGTA) exist. These results indicated that activation of JAK1, JAK2 and STAT3 is necessary for leptin-induced transactivation of NPY gene through the leptin-response element in these neural cells.lld:pubmed
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pubmed-article:12590942pubmed:articleTitleLeptin-induced transactivation of NPY gene promoter mediated by JAK1, JAK2 and STAT3 in the neural cell lines.lld:pubmed
pubmed-article:12590942pubmed:affiliationDivision of Pharmacology, Department of Molecular Genetics, Course for Molecular and Cellular Medicine, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Niigata 951 8510, Japan.lld:pubmed
pubmed-article:12590942pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:12590942pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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