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dc.contributor.author이영한-
dc.date.accessioned2021-02-17T05:25:55Z-
dc.date.available2021-02-17T05:25:55Z-
dc.date.issued2001-03-
dc.identifier.citationJOURNAL OF BIOLOGICAL CHEMISTRY, v. 276, issue. 11, page. 7797-7805en_US
dc.identifier.issn0021-9258-
dc.identifier.urihttps://www.sciencedirect.com/science/article/pii/S0021925819321180-
dc.identifier.urihttps://repository.hanyang.ac.kr/handle/20.500.11754/158598-
dc.description.abstractThe early growth response gene-1 (Egr-1) is a transcription factor that plays an important role in cell growth and differentiation. It has been known that Egr-1 expression is down-regulated in many types of tumor tissues, including human fibrosarcoma HT1080 cells, and introduction of the Egr-1gene into HT1080 cells inhibits cell growth and tumorigenic potential. Trifluoperazine (TFP), a phenothiazine class calmodulin antagonist, is known to inhibit DNA synthesis and cell proliferation and potentially important in antitumor activities. To understand the regulatory mechanism of Egr-1, we investigated the effect of TFP on expression of Egr-1 in HT1080 cells. Herein, we report thatEgr-1 expression was increased by TFP in synergy with serum at the transcriptional level. Both the Ca2+/calmodulin-dependent protein kinase II inhibitor KN62 and the calcineurin inhibitor cyclosporin A enhanced TFP-dependent increase of Egr-1, suggesting that the Ca2+/calmodulindependent pathway plays a role in regulation of Egr-1 expression in HT1080 cells. The TFP-stimulated increase of the Egr-1 protein was preferentially inhibited by the MEK-specific inhibitor PD98059. In addition, activation of human Egr-1 promoter and the transcriptional activation of the ternary complex factor Elk-1 induced by TFP were inhibited both by pretreatment of PD98059 and by expression of the dominant-negative RasN17. These results indicate that the Ras/MEK/Erk/Elk-1 pathway is necessary for TFP-inducedEgr-1 expression. We propose that the calmodulin antagonist TFP stimulates Egr-1 gene expression by modulating Ras/MEK/Erk and activation of the Elk-1 pathway in human fibrosarcoma HT1080 cells.en_US
dc.language.isoen_USen_US
dc.publisherAMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INCen_US
dc.titleInduction of Early Growth Response-1 Gene Expression by Calmodulin Antagonist Trifluoperazine through the Activation of Elk-1 in Human Fibrosarcoma HT1080 Cellsen_US
dc.typeArticleen_US
dc.identifier.doi10.1074/jbc.M009465200-
dc.relation.journalJOURNAL OF BIOLOGICAL CHEMISTRY-
dc.contributor.googleauthorShin, S.Y.-
dc.contributor.googleauthorKim, S.-Y.-
dc.contributor.googleauthorKim, J.-H.-
dc.contributor.googleauthorLee, Y.H.-
dc.contributor.googleauthorMin, D.S.-
dc.contributor.googleauthorKo, J.-
dc.contributor.googleauthorKang, U.-G.-
dc.contributor.googleauthorKim, Y.S.-
dc.contributor.googleauthorKwon, T.K.-
dc.contributor.googleauthorHan, M.Y.-
dc.contributor.googleauthorKim, Y.H.-
dc.relation.code2009204730-
dc.sector.campusE-
dc.sector.daehakCOLLEGE OF SCIENCE & TECHNOLOGY[E]-
dc.sector.departmentDIVISION OF MOLECULAR & LIFE SCIENCE-
dc.identifier.pidyounghan-
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COLLEGE OF SCIENCE AND CONVERGENCE TECHNOLOGY[E](과학기술융합대학) > ETC
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