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http://ir.cmu.edu.tw/ir/handle/310903500/29244
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| 題名: | Polymorphism for transforming growth factor beta 1-509 (TGF-B1-509): Association with endometriosis |
| 作者: | Hsieh, YY;Chang, CC;Tsai, FJ;Peng, CT;Yeh, LS;Lin, CC |
| 貢獻者: | 附設醫院兒科部;China Med Univ Hosp, Dept Pediat & Med Genet, Taichung, Taiwan;China Med Univ Hosp, Dept Obstet & Gynecol, Taichung, Taiwan;China Med Univ Hosp, Dept Family Med, Taichung, Taiwan;Natl Chiao Tung Univ, Dept Biol Sci & Technol, Hsinchu, Taiwan |
| 日期: | 2005 |
| 上傳時間: | 2010-09-24 14:28:30 (UTC+8) |
| 出版者: | SPRINGER/PLENUM PUBLISHERS |
| 摘要: | The prion diseases or transmissible spongiform encephalopathy, such as human Creutzfeldt-Jakob disease (CJD) and so-called mad cow disease, are attributed to the causative agent, the scrapie variant of prion protein (PrPSc) which causes fatal neurodegeneration. To investigate if stresses such as nitric oxide (NO) induced the cellular isoform of prion protein (PrPC), lipopolysaccharide, and sodium nitroprusside were used to treat N2a and NT2 cells, which resulted in elevated levels of the PRNP mRNA and prion protein. The signaling pathway for the NO-induced PrPC production involved guanylyl cyclase, MEK, and p38 MAPK as shown by the effect of specific pharmacological inhibitors ODQ, PD98059, and SB203580, respectively. Knowing the PrP induction by the biologically existing stimulus, this study provides useful information about the possible cellular mechanism and strategies for the treatment of CJD. (c) 2005 Elsevier Inc. All rights reserved. |
| 關聯: | BIOCHEMICAL GENETICS 43(5月6日):203-210 |
| 顯示於類別: | [台中附設醫院] 期刊論文
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