Full metadata record
DC Field | Value | Language |
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dc.contributor.author | 전길자 | - |
dc.date.accessioned | 2018-05-18T08:15:05Z | - |
dc.date.available | 2018-05-18T08:15:05Z | - |
dc.date.issued | 2005 | - |
dc.identifier.issn | 0950-9232 | - |
dc.identifier.other | OAK-2743 | - |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/243134 | - |
dc.description.abstract | Since 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.language | English | - |
dc.title | HSP25 inhibits radiation-induced apoptosis through reduction of PKCδ-mediated ROS production | - |
dc.type | Article | - |
dc.relation.issue | 23 | - |
dc.relation.volume | 24 | - |
dc.relation.index | SCIE | - |
dc.relation.index | SCOPUS | - |
dc.relation.startpage | 3715 | - |
dc.relation.lastpage | 3725 | - |
dc.relation.journaltitle | Oncogene | - |
dc.identifier.doi | 10.1038/sj.onc.1208440 | - |
dc.identifier.wosid | WOS:000229346300003 | - |
dc.identifier.scopusid | 2-s2.0-19844377667 | - |
dc.author.google | Lee Y.-J. | - |
dc.author.google | Lee D.-H. | - |
dc.author.google | Cho C.-K. | - |
dc.author.google | Chung H.-Y. | - |
dc.author.google | Bae S. | - |
dc.author.google | Jhon G.-J. | - |
dc.author.google | Soh J.-W. | - |
dc.author.google | Jeoung D.-I. | - |
dc.author.google | Lee S.-J. | - |
dc.author.google | Lee Y.-S. | - |
dc.contributor.scopusid | 전길자(6701488476) | - |
dc.date.modifydate | 20180517114531 | - |