ZAK inhibits human lung cancer cell growth via ERK and JNK activation in an AP-1-dependent manner
スポンサーリンク
概要
- 論文の詳細を見る
- 2010-06-10
著者
-
YANG Jaw-Ji
Institute of Oral Biology & Biomaterial Science, Chung Shan Medical University
-
LEE Yi-Ju
Institute of Immunology, Chung Shan Medical University
-
HUNG Hsin-Hung
Institute of Medical & Molecular Toxicology, Chung Shan Medical University
-
TSENG Wei-Pu
Institute of Medical & Molecular Toxicology, Chung Shan Medical University
-
TU Chuan-Chou
Division of Chest Medicine, Department of Internal Medicine, Armed Force Taichung General Hospital
-
LEE Huei
Institute of Medical & Molecular Toxicology, Chung Shan Medical University
-
WU Wen-Jun
Institute of Medical & Molecular Toxicology, Chung Shan Medical University
-
Lee Yi-ju
Institute Of Immunology Chung Shan Medical University
-
Wu Wen-jun
Institute Of Medical & Molecular Toxicology Chung Shan Medical University
-
Yang Jaw-ji
Institute Of Oral Biology & Biomaterial Science Chung Shan Medical University
-
Tseng Wei-pu
Institute Of Medical & Molecular Toxicology Chung Shan Medical University
-
Tu Chuan-chou
Division Of Chest Medicine Department Of Internal Medicine Armed Force Taichung General Hospital
-
Hung Hsin-hung
Institute Of Medical & Molecular Toxicology Chung Shan Medical University
関連論文
- ZAK inhibits human lung cancer cell growth via ERK and JNK activation in an AP-1-dependent manner
- Exposure to Mosquito Coil Smoke May be a Risk Factor for Lung Cancer in Taiwan
- Apicidin-Resistant HA22T Hepatocellular Carcinoma Cells strongly activated the Wnt/β-Catenin Signaling Pathway and MMP-2 Expression via the IGF-IR/PI3K/Akt Signaling Pathway Enhancing Cell Metastatic Effect