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Proteasome-dependent Degradation of Cyclin D1 in 1-Methyl-4-phenylpyridinium Ion (MPP+)-induced Cell Cycle Arrest
https://repo.qst.go.jp/records/44246
https://repo.qst.go.jp/records/44246f9410ea0-cb27-405a-ab70-0cc4b4e3f1dd
Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2006-06-13 | |||||
タイトル | ||||||
タイトル | Proteasome-dependent Degradation of Cyclin D1 in 1-Methyl-4-phenylpyridinium Ion (MPP+)-induced Cell Cycle Arrest | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
アクセス権 | ||||||
アクセス権 | metadata only access | |||||
アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
著者 |
Jie, Bai
× Jie, Bai× Nakamura, Hajime× Ueda, Shugo× Kwon, Yong-Won× Tanaka, Toru× Ban, Sadayuki× Yodoi, Junji× 伴 貞幸 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | 1-Methyl-4-phenylpyridinium ion (MPP+), an active metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, induces cell death and inhibition of cell proliferation in various cells. However, the mechanism whereby MPP+ inhibits cell proliferation is still unclear. In this study, we found that MPP+ suppressed the proliferation with accumulation in G1 phase without inducing cell death in p53-deficient MG63 osteosarcoma cells. MPP+ induced hypophosphorylation of retinoblastoma protein and rapidly down-regulated the protein but not mRNA levels of cyclin D1 in MG63 cells. The down-regulation of cyclin D1 protein was suppressed by a proteasome inhibitor, MG132. The cyclin D1 down-regulation by MPP+ was also observed in p53-positive PC12, HeLa S3, and HeLa 0 cells, which are a subclone of HeLa S3 lacking mitochondrial DNA. Moreover, MPP+ dephosphorylated Akt in PC12 cells, which was rescued by the pretreatment with nerve growth factor. In addition, the pretreatment with nerve growth factor or lithium chloride, a glycogen synthase kinase-3 inhibitor, suppressed the cyclin D1 down-regulation caused by MPP+. Our results demonstrate that MPP+ induces cell cycle arrest independently of its mitochondrial toxicity or the p53 status of the target cells, but rather through the proteasome- and phosphatidylinositol 3-Akt-glycogen synthase kinase-3-dependent cyclin D1 degradation. | |||||
書誌情報 |
The Journal of Biological Chemistry 巻 279, 号 37, p. 38710-38714, 発行日 2004-09 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 0021-9258 |