Full metadata record

DC Field Value Language
dc.contributor.authorKyoung-Jin Min-
dc.contributor.authorHee Jung Um-
dc.contributor.authorSeung Un Seo-
dc.contributor.authorSeon Min Woo-
dc.contributor.authorShin Kim-
dc.contributor.authorJong-Wook Park-
dc.contributor.authorHyun-Shik Lee-
dc.contributor.authorSang Hyun Kim-
dc.contributor.authorYung Hyun Choi-
dc.contributor.authorTae-Jin Lee-
dc.contributor.authorTaeg Kyu Kwon-
dc.date.accessioned2019-03-11T16:30:53Z-
dc.date.available2019-03-11T16:30:53Z-
dc.date.issued2018-
dc.identifier.citationDrug Development Research, Vol.79(1) : 3-10, 2018-
dc.identifier.issn0272-4391-
dc.identifier.otheroak-2018-0110-
dc.identifier.urihttp://kumel.medlib.dsmc.or.kr/handle/2015.oak/41070-
dc.description.abstractPreclinical Research & Development Angelicin is a furocoumarin derived from Psoralea corylifolia L. fruit that has anti-inflammatory and anti-tumor activity. In the present study, the effect of angelicin in enhancing tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptotic cell death was studied in Caki (renal carcinoma) cells. Angelicin alone and TRAIL alone had no effect on apoptosis, but in combination these compounds markedly induced apoptosis in the cancer cell lines while not inducing apoptosis in normal cells. The combination treatment induced accumulation of the sub-G1 population, DNA fragmentation, and activated caspase 3 activity in Caki cells, induced down-regulation of c-FLIP expression post-translationally, and over-expression of c-FLIP markedly blocked apoptosis induced by combined treatment with angelicin plus TRAIL. This study provides evidence that angelicin might be a TRAIL sensitizer.-
dc.description.statementofresponsibilityopen-
dc.publisherSchool of Medicine (의과대학)-
dc.rightsBY_NC_ND-
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/2.0/kr-
dc.subjectTRAIL-
dc.subjectangelicin-
dc.subjectapoptosis-
dc.subjectc-FLIP-
dc.subjectcaspase-
dc.titleAngelicin potentiates TRAIL-induced apoptosis in renal carcinoma Caki cells through activation of caspase 3 and down-regulation of c-FLIP expression-
dc.typeArticle-
dc.contributor.localauthor김신-
dc.contributor.localauthor박종욱-
dc.contributor.localauthor권택규-
dc.contributor.alternativelocalauthorKim, Shin-
dc.contributor.alternativelocalauthorKwon, Taeg Kyu-
dc.contributor.alternativelocalauthorPark, Jong Wook-
dc.contributor.departmentDept. of Immunology (면역학)-
dc.citation.volume79-
dc.citation.number1-
dc.citation.startpage3-
dc.citation.titleDrug Development Research-
dc.citation.endpage10-
dc.identifier.doi10.1002/ddr.21414-


qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

BROWSE