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- W2004871569 abstract "Neuropeptide 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." @default.
- W2004871569 created "2016-06-24" @default.
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- W2004871569 date "2003-06-01" @default.
- W2004871569 modified "2023-09-23" @default.
- W2004871569 title "Leptin-induced transactivation of NPY gene promoter mediated by JAK1, JAK2 and STAT3 in the neural cell lines" @default.
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- W2004871569 doi "https://doi.org/10.1016/s0197-0186(02)00160-2" @default.
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