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dc.contributor.author전길자-
dc.date.accessioned2018-05-18T08:15:05Z-
dc.date.available2018-05-18T08:15:05Z-
dc.date.issued2005-
dc.identifier.issn0950-9232-
dc.identifier.otherOAK-2743-
dc.identifier.urihttp://dspace.ewha.ac.kr/handle/2015.oak/243134-
dc.description.abstractSince radiation-induced caspase-dependent apoptosis and ROS generation were partially prevented by HSP25 overexpression, similar to the treatment of control cells with antioxidant agents such as DPI and tiron, questions arise whether radiation-mediated ROS generation contributes to the apoptotic cell death, and also whether HSP25 overexpression can reduce ROS mediated apoptotic cell death. In the present study, radiation-induced cytochrome c release from mitochondria and activation of caspases accompanied by a decrease of mitochondrial membrane potential in Jurkat T cells were shown to be inhibited by mitochondrial complex I inhibitor rotenone, suggesting that mitochondrial ROS might be important in radiation-induced caspase-dependent apoptosis. When HSP25 was overexpressed, effects similar to the treatment of cells with the antioxidants were obtained, indicating that HSP25 suppressed radiation-induced mitochondrial alteration that resulted in apoptosis. Furthermore, activation of p38 MAP kinase by radiation was associated with radiation-induced cell death and ROS production and PKCδ was an upstream molecule for p38 MAP kinase activation, ROS generation and subsequent caspase-dependent apoptotic events. However, in the HSP25 overexpressed cells, the above-described effects were blocked. In fact, radiation-induced membrane translocation of PKCδ and tyrosine phosphorylation were inhibited by HSP25. Based on the above data, we suggest that HSP25 downregulates PKCδ, which is a key molecule for radiation-induced ROS generation and mitochondrial-mediated caspase-dependent apoptotic events. © 2005 Nature Publishing Group All rights reserved.-
dc.languageEnglish-
dc.titleHSP25 inhibits radiation-induced apoptosis through reduction of PKCδ-mediated ROS production-
dc.typeArticle-
dc.relation.issue23-
dc.relation.volume24-
dc.relation.indexSCI-
dc.relation.indexSCIE-
dc.relation.indexSCOPUS-
dc.relation.startpage3715-
dc.relation.lastpage3725-
dc.relation.journaltitleOncogene-
dc.identifier.doi10.1038/sj.onc.1208440-
dc.identifier.wosidWOS:000229346300003-
dc.identifier.scopusid2-s2.0-19844377667-
dc.author.googleLee Y.-J.-
dc.author.googleLee D.-H.-
dc.author.googleCho C.-K.-
dc.author.googleChung H.-Y.-
dc.author.googleBae S.-
dc.author.googleJhon G.-J.-
dc.author.googleSoh J.-W.-
dc.author.googleJeoung D.-I.-
dc.author.googleLee S.-J.-
dc.author.googleLee Y.-S.-
dc.contributor.scopusid전길자(6701488476)-
dc.date.modifydate20180517114531-
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