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방사선에 의한 Apoptosis에서 Fas의 역할

DC FieldValueLanguage
dc.contributor.author성진실-
dc.date.accessioned2016-05-16T11:22:14Z-
dc.date.available2016-05-16T11:22:14Z-
dc.date.issued2002-
dc.identifier.issn1229-8719-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/144400-
dc.description.abstractPurpose: It has been recognized that interaction of the Fas : Fas ligand plays an important role in radiation-induced apoptosis. The purpose of this study was to investigate the role of Fas mutation in radiation-induced apoptosis in vivo. Materials and Methods: Mice with mutations in Fas, MRL/Mpj-Faslpr, and its normal control, MRL/Mpj, were used in this study. Eight-week old male mice were given whole body radiation. After irradiation, the mice were killed and their spleens were collected at different time intervals. Tissue samples were stained with hematoxylin-eosin and the numbers of apoptotic cells were scored. Regulating molecules of apoptosis including p53, Bcl-2, Bax, Bcl-XL, and Bcl-XS were also analyzed by Western blotting. Results: At 25 ㏉ irradiation, the level of apoptosis reached the peak value at 8 hr after radiation and recovered to the normal value at 24 hr after radiation in MRL/Mpj mice. In contrast, the peak apoptosis level appeared at 4 hr after radiation in MRL/Mpj-Faslpr mice. At 8 hr after radiation, the levels of apoptosis in MRL/Mpj mice and MRL/Mpj-Faslpr mice were 52.3±7.8% and 8.0±8.6%, respectively (p<0.05). The expression of apoptosis regulating molecules, p53, Bcl-XL and Bcl-XS, increased in MRL/Mpj mice in response to radiation; p53 with a peak level of 3-fold at 8 h, Bcl-XL with a peak level of 3.3-fold at 12 h, and Bcl-XS with a peak level of 3-fold at 12h after 25 ㏉ radiation. Bcl-2 and Bax did not show significant change in MRL/Mpj mice. However in MRL/Mpj-Faslpr mice, the expression levels of p53, Bcl-2, Bax, Bcl-XL and Bcl-XS showed no significant change. Conclusion: The level of radiation-induced apoptosis was lower in Fas mutated mice, lpr, than in control mice. This seemed to be related to the lack of radiation-induced p53 activation in the lpr mice. This result suggests that Fas plays an important role in radiation-induced apoptosis in vivo.-
dc.description.statementOfResponsibilityopen-
dc.format.extent246~252-
dc.languageKorean-
dc.publisher대한방사선종양학회-
dc.relation.isPartOfJournal of the Korean Society for Therapeutic Radiology and Oncology-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.title방사선에 의한 Apoptosis에서 Fas의 역할-
dc.title.alternativeThe Role of Fas in Radiation Induced Apoptosis in vivo-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Radiation Oncology (방사선종양학)-
dc.contributor.googleauthor김성희-
dc.contributor.googleauthor성진실-
dc.contributor.googleauthor성제경-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA01956-
dc.relation.journalcodeJ01857-
dc.subject.keyword방사선-
dc.subject.keywordApoptosis-
dc.subject.keywordFas-
dc.subject.keywordIpr-
dc.contributor.alternativeNameSeong, Jin Sil-
dc.contributor.affiliatedAuthorSeong, Jin Sil-
dc.rights.accessRightsfree-
dc.citation.volume20-
dc.citation.number3-
dc.citation.startPage246-
dc.citation.endPage252-
dc.identifier.bibliographicCitationJournal of the Korean Society for Therapeutic Radiology and Oncology, Vol.20(3) : 246-252, 2002-
dc.identifier.rimsid49680-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Radiation Oncology (방사선종양학교실) > 1. Journal Papers

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