To Investigate the Role of BNIP3 at NO-Induced Cell Death in N2A Cells and Hypoxia in HEK293T Cells

• Main Authors: Yin, Chieh-Fan, 鄞偈帆
• Other Authors: Tang, Shye-Jye
• Format: Others
• Language: zh-TW
• Published: 2014
• Online Access: http://ndltd.ncl.edu.tw/handle/hdz3xh

碩士 === 國立臺灣海洋大學 === 生物科技研究所 === 102 === Oxygen homeostasis in biological evolution, development, physiology, and even pathology. Generally in the case of hypoxia, there is a common physiologically and pharmacologically: coronary artery disease, the peripheral artery disease, aging, neurodegenerative diseases and cancer. Where in the cancer, the area where hypoxia increases the rate of cancer cell proliferation, but also accompanied by abnormal vascular function generation. In hypoxia, hypoxia-inducible factors (HIFs) will play as transcriptional activators to regulate oxygen homeostasis. Previously studys in many human cancer cells, hypoxia induces mitochondrial autophagy through BNIP3 expression of HIF-1-dependent. BNIP3-induced autophagy is considered relate to hypoxia-induced cell death, paper indicates that the general organization in the face of hypoxia will be a substantial up-regulate BNIP3, but in some tumor cells will reduce BNIP3 expression, avoid cell death; while but it will autophagy induced by mitochondrial BNIP3 in some cells adapt to hypoxia. Previous results indicated that, tyrosine phosphorylation sites on BNIP3 will affect its stability, dimer formed or not, or even a position of the distribution cell. So our study is to investigate whether the tyrosine phosphorylation sites on BNIP3 affects reaction cells in hypoxia.