摘要或動機

細胞凋亡具有控制生物體細胞數目之功能，能讓特定的細胞走向死亡，因此若能掌握其作用機制，便可能藉由調控細胞凋亡的發生，進而應用於癌症治療。前人研究（2.）指出，經基因重組技術純化之口蹄疫病毒鞘蛋白rVP1，會導致BHK-21的Akt 蛋白質去活化，引起細胞凋亡的現象。然而在其後續的研究中，卻發現到在BHK-21中大量表現磷酸化的Akt 蛋白質，並無法反轉由rVP1 所誘發之細胞凋亡。因此本實驗利用二維蛋白質電泳，尋找Akt pathway 以外之細胞凋亡相關蛋白質。目前已證明Prohibitin 此一蛋白質，在由rVP1 所引起之細胞凋亡中，有自細胞核移動至細胞質的現象。此外，亦經由實驗排除Prohibitin 位於Akt pathway 的可能性。Western Blot 之結果更顯示，經rVP1 處理後，Prohibitin 在很短的時間內便出現遷移的現象，故推測其具有調控細胞凋亡上游反應的功能。Apoptosis can lead some specific cells to programmed death, thus, it is a major way for creatures to control their cells amounts. If we can command the mechanism of apoptosis, we may use it as a therapy for cancer by artificial regulation of apoptosis. VP1 is one of the capsid proteins of Foot and Mouth Disease Virus (FMDV). A research (2.) has indicated that the recombinant VP1 (rVP1) can result in dephosphorylation of Akt in BHK-21, and then lead the cells to apoptosis. However, in their follow-up experiments, they discovered that even if they expressed great amount of phospho-Akt in BHK-21, it still couldn’t reverse the apoptosis induced by rVP1. Therefore, this experiment takes the advantage of two-dimension protein electrophoresis (2D) in order to find apoptotic proteins excluded from the Akt pathway. I have found that Prohibitin exports from nucleus to cytosol after rVP1 treatment. Furthermore, I eliminate the possibility that Prohibitin’s may be located in Akt pathway. The results of Western Blot also shows that protein amount of Prohibitin in BHK-21 increase after rVP1 treatment, hence the purpose of nuclear export of Prohibitin might not be to degrade it. It might have some much more important function in the process of exportation. Besides, Prohibitin exports to cytosol in quite a short time after rVP1 treatment. According to this phenomenon, I suppose that Prohibitin has a role as a regulator of apoptotic up-stream reactions.