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Retinoic Acid激活Akt、Rac1、與抗氧化酵素並促進神經細...

國立高雄大學生物科技研究所

Retinoic Acid激活Akt、Rac1、與抗氧化酵素並促進神經細胞Neuro-2a存活之研究 = Study of retinoic acid activating Rac1, Akt and anti-oxidant enzymes to induce survival of Neuro-2a cell line

紀錄類型:	書目-語言資料,印刷品 : 單行本
並列題名:	Study of retinoic acid activating Rac1, Akt and anti-oxidant enzymes to induce survival of Neuro-2a cell line
作者:	陳映端,
其他團體作者:	國立高雄大學
出版地:	[高雄市]
出版者:	撰者;
出版年:	2012[民101]
面頁冊數:	77面圖，表 : 30公分;
標題:	神經細胞存活
標題:	neuronal survival
電子資源:	http://handle.ncl.edu.tw/11296/ndltd/12935328527180686427
附註:	106年4月25日公開
附註:	參考書目：面66-73
摘要註:	在神經細胞存活的研究中，Akt 為其中一項重要的指標，尤其是適當磷酸化的Akt，簡稱phospho-Akt，縮寫為p-Akt，參與許多生化反應。過多的活性氧系物質，即reactive oxygen species，縮寫成ROS，會對神經細胞產生傷害，而細胞則有SOD(superoxide dismutase)、Catalase 和glutathione peroxidase 的抗氧化酵素來抵抗ROS的傷害。為了釐清神經細胞中抗氧化酵素與存活的關係，本研究使用Neuro-2a 細胞株來進行探討，藉由轉染不同的Rac1 基因，分別為wild type 的Rac1、持續活化的G12V 和呈現不活化的T17N，及處理10μM Retinoic acid，簡稱為RA，刺激神經細胞分化，來進一步探討細胞存活與抗氧化酵素間的訊息傳遞關係；由實驗結果得知，轉染Rac1 及G12V 基因皆會促進突觸伸出，而T17N 則是抑制的情形，另外轉染不同的Rac1 基因，細胞內p-Akt、SOD1、Catalase 的蛋白質表現會提昇，但對Akt、SOD2 卻沒有影響。另外，以免疫沈澱實驗證明Akt 是直接透過Rac1 去調控細胞突觸生長，並且當Rac1 活化時會提昇與Catalase 的結合；此外Akt 也會2藉由c-Src 蛋白質與SOD1 結合。以上總結，在RA 所引起神經細胞的分化，細胞內是由Akt/ Rac1 這條訊息傳遞路徑去調控，其中抗氧化酵素的SOD1 與Catalase也會參與其中，並且透過Rac1 與Catalase 結合，證明存活路徑與抗氧化酵素間的訊息傳遞關係。 Akt plays an important role in neuronal survival, especially phosphorylated Akt. Additionally, there are reports that excess ROS (reactive oxygen species) can damage neuronal cells. However, the damage can be prevented by anti-oxidant enzymes such as SOD (superoxide dismutase), Catalase, and glutathione peroxidase. In order to realize the relationship between anti-oxidant enzymes and survival signal, Neuro-2a cell line was used in this research. Three different Rac1 genes were transfected into cells, including wild type Rac1, constitutive activated G12V, and dominant negative T17N. After transfecting, 10μM Retinoic acid (RA) was treated to induce neurite outgrowth. In this research, neurite outgrowth was found in Rac1 wild type and G12V, but not T17N. Protein expressions of p-Akt, SOD1 and Catalase were increased in all transfection treatments, but not Akt and SOD2. In the assay of immunoprecipitation, Rac1 could bind to Akt and induced neurite outgrowth. RA-induced Rac1 enhanced its binding with Catalase. Furthermore, Akt was associated with SOD1 via c-Src. In summary, RA-induced neurite outgrowth was regulated by Akt/ Rac1 pathway. SOD1 and Catalase involved in RA-induced neurite outgrowth. The relationship between survival pathway and anti-oxidant enzymes relied on the association of Rac1 and Catalase.

Retinoic Acid激活Akt、Rac1、與抗氧化酵素並促進神經細胞Neuro-2a存活之研究 = Study of retinoic acid activating Rac1, Akt and anti-oxidant enzymes to induce survival of Neuro-2a cell line
陳, 映端

Retinoic Acid激活Akt、Rac1、與抗氧化酵素並促進神經細胞Neuro-2a存活之研究 = Study of retinoic acid activating Rac1, Akt and anti-oxidant enzymes to induce survival of Neuro-2a cell line / 陳映端撰 - [高雄市] : 撰者, 2012[民101]. - 77面 ; 圖，表 ; 30公分.
106年4月25日公開參考書目：面66-73.
神經細胞存活neuronal survival

Retinoic Acid激活Akt、Rac1、與抗氧化酵素並促進神經細胞Neuro-2a存活之研究 = Study of retinoic acid activating Rac1, Akt and anti-oxidant enzymes to induce survival of Neuro-2a cell line
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