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資料載入中.....
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請使用永久網址來引用或連結此文件:
http://ir.cmu.edu.tw/ir/handle/310903500/30199
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| 題名: | The fixed combination of fortified vancomycin and amikacin ophthalmic solution-VA solution - In vitro study of the potency and stability |
| 作者: | Lin, JM;Tsai, YY;Fu, YL |
| 貢獻者: | 附設醫院眼科部;China Med Univ Hosp, Dept Ophthalmol, Taichung 404, Taiwan;Chung Shan Med Univ, Inst Biochem, Taichung, Taiwan |
| 日期: | 2005 |
| 上傳時間: | 2010-09-24 14:50:59 (UTC+8) |
| 出版者: | LIPPINCOTT WILLIAMS & WILKINS |
| 摘要: | beta-catenin is upregulated in many human cancers and considered to be an oncogene. Hepatocellular carcinoma (HCC) is one of the most prevalent human malignancies, and individuals who are chronic hepatitis B virus (HBV) carriers have a greater than 100-fold increased relative risk of developing HCC. Here we report a mechanism by which HBV-X protein (HBX) upregulates beta-catenin. Erk, which is activated by HBX, associates with GSK-3 beta through a docking Motif ((FKFP)-F-291) of GSK-3 beta and phosphorylates GSK-3 beta at the (43)Thr residue, which primes GSK-3 beta for its subsequent phosphorylation at Ser9 by p90RSK, resulting in inactivation of GSK-3 beta and upregulation of P-catenin. This pathway is a general signal, as it was also observed in cell lines in which Erk-primed inactivation of GSK-3 beta was regulated by IGF-1, TGF-beta, and receptor tyrosine kinase HER2, and is further supported by immunohistochemical staining in different human tumors, including cancers of the liver, breast, kidney, and stomach. |
| 關聯: | CORNEA 24(6):717-721 |
| 顯示於類別: | [台中附設醫院] 期刊論文
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