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dc.contributor.author이경림*
dc.date.accessioned2016-10-15T01:10:23Z-
dc.date.available2016-10-15T01:10:23Z-
dc.date.issued2009*
dc.identifier.issn0003-9861*
dc.identifier.otherOAK-5595*
dc.identifier.urihttps://dspace.ewha.ac.kr/handle/2015.oak/232415-
dc.description.abstractWe reported previously that translationally controlled tumor protein (TCTP) is a cytoplasmic repressor of Na,K-ATPase in HeLa cells. In the current study, we showed that TCTP overexpression using adenovirus as vehicle, induced partial inhibition of Na,K-ATPase; phosphorylation of EGFR tyrosine residues 845, 992, 1068, and 1148; activation of Ras/Raf/ERK pathway; activation of PI3K/Akt pathway; and phosphorylation of PLC-γ in HeLa cells. Specific inhibition of PI3K/Akt pathway in contrast to the inhibition of ERK, significantly decreased TCTP overexpression-induced survival signal. Inhibition of PLC-γ pathway significantly decreased TCTP overexpression-induced cell migration but inhibition of ERK had less effect. These results suggest that TCTP plays a key physiological role in cell survival through Akt pathway and migration through PLC-γ pathway. © 2009 Elsevier Inc. All rights reserved.*
dc.languageEnglish*
dc.titleRoles of ERK, PI3 kinase, and PLC-γ pathways induced by overexpression of translationally controlled tumor protein in HeLa cells*
dc.typeArticle*
dc.relation.issue1*
dc.relation.volume485*
dc.relation.indexSCI*
dc.relation.indexSCIE*
dc.relation.indexSCOPUS*
dc.relation.startpage82*
dc.relation.lastpage87*
dc.relation.journaltitleArchives of Biochemistry and Biophysics*
dc.identifier.doi10.1016/j.abb.2009.02.002*
dc.identifier.wosidWOS:000265754100012*
dc.identifier.scopusid2-s2.0-64549105686*
dc.author.googleKim M.*
dc.author.googleJung J.*
dc.author.googleLee K.*
dc.contributor.scopusid이경림(7501517435)*
dc.date.modifydate20240501081003*
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약학대학 > 약학과 > Journal papers
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