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dc.contributor.authorPark, Rackhyun-
dc.contributor.authorHà, Thị Kim Quy-
dc.contributor.authorPark, Junsoo-
dc.contributor.authorJang, Minsu-
dc.contributor.authorLee, Kang Il-
dc.contributor.authorOh, Won Keun-
dc.contributor.authorKim, Hyunju-
dc.date.accessioned2018-11-21T11:26:05Z-
dc.date.available2018-11-21T11:26:05Z-
dc.date.issued2017-
dc.identifier.urihttp://localhost:8080//jspui/handle/123456789/5247-
dc.description.abstractReserpine is a well-known medicine for the treatment of hypertension, however the role of reserpine in cell signaling is not fully understood. Here, we report that reserpine treatment induces the phosphorylation of AMP activated protein kinase (AMPK) at threonine 172 (T172) in PC12 cells. Phosphorylation of AMPK T172 is regulated by upstream signaling molecules, and the increase of phospho-T172 indicates that AMPK is activated. When we examined the FOXO3a dependent transcription by using the FHRE-Luc reporter assay, reserpine treatment repressed the FHRE-Luc reporter activity in a dose dependent manner. Finally, we showed that reserpine treatment induced the phosphorylation of AMPK as well as cell death in MCF-7 cells. These results suggest that AMPK is a potential cellular target of reserpine.vi_VN
dc.language.isoenvi_VN
dc.relation.ispartofseriesNatural Product Sciences;23 .- p.157-161-
dc.subjectReserpinevi_VN
dc.subjectAMPKvi_VN
dc.subjectFOXO3avi_VN
dc.subjectPC12vi_VN
dc.subjectMCF-7vi_VN
dc.titleReserpine treatment activates AMP activated protein kinase (AMPK)vi_VN
dc.typeArticlevi_VN
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