English  |  正體中文  |  简体中文  |  全文筆數/總筆數 : 45073/58249 (77%)
造訪人次 : 2425436      線上人數 : 152
RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
搜尋範圍 查詢小技巧：
  • 您可在西文檢索詞彙前後加上"雙引號"，以獲取較精準的檢索結果
  • 若欲以作者姓名搜尋，建議至進階搜尋限定作者欄位，可獲得較完整資料
    •  進階搜尋


    請使用永久網址來引用或連結此文件: http://libir.tmu.edu.tw/handle/987654321/5835


    題名: Mcl-1蛋白之功能解析 -由找尋其交互作用之蛋白探討
    Functional characterization of Mcl-1 by searching for Mcl-1 interacting proteins
    作者: 李如鑠
    Ru-Shuo Lee
    貢獻者: 細胞及分子生物研究所
    關鍵詞: 細胞凋亡
    交互作用蛋白
    apoptosis
    interacting protein
    日期: 2000
    上傳時間: 2009-09-11 15:44:26 (UTC+8)
    摘要: Mcl-1屬於Bcl-2家族蛋白質之一，而此家族成員多參與調控細胞凋亡的過程。Mcl-1如同其他Bcl-2家族成員一樣，擁有相似的BH1、BH2、BH3以及膜鑲嵌區域。先前的研究指出，Mcl-1是血癌細胞分化過程中引發的一個蛋白。最近也發現Mcl-1在granulocyte macrophage colony-stimulating factor (GM-CSF) 及interleukin 3 (IL-3) 所引發的細胞存活反應中扮演一重要角色。在一些研究中證明了不同抗細胞死亡及促進細胞死亡的Bcl-2相關蛋白質之間的交互作用對於決定細胞的命運上是十分關鍵性的的。例如當Bax與Bcl-2形成異構物 (heterodimer) 時便會中和Bax促進細胞凋亡的能力。相同的，Mcl-1也會與一些Bcl-2家族成員形成異構物，如Bok、Bax、Bak 及Bik。在此篇研究中，我透過Yeast two hybrid方法來找尋Mcl-1在淋巴球中之交互作用蛋白，藉以了解Mcl-1在此系統中之功能。藉由篩選淋巴球cDNA library，我發現了58個候選蛋白可能會與Mcl-1進行交互作用，其中包括了Bcl-2家族成員Bax、Bid及Bik。我也發現了一些未被確定的人類基因，名為KIAA0147，KIAA0719以及TPT1亦會與Mcl-1進行交互作用。在試管內的GST-pull down研究中顯示KIAA0719及TPT1會與Mcl-1交互作用，但KIAA0147並不會。未來將進一步探討是否Mcl-1會與KIAA0719及TPT1在細胞內進行交互作用。
    Mcl-1 belongs to the Bcl-2 protein family whose members participate in the regulation of apoptosis. It shares homologous BH1, BH2, BH3 and transmembrane domain with other Bcl-2 family members. Previous studies showed that Mcl-1 is induced during differentiation of leukemic cells. It was recently demonstrated that Mcl-1 is one of the survival components elicited by granulocyte macrophage colony-stimulating factor (GM-CSF) and interleukin 3 (IL-3). Some studies demonstrated that interaction between different anti- and pro-apoptotic Bcl-2 related proteins are critical in the determination of cell fate. For example, neutralization of pro-apoptotic activity of Bax occurred when it heterodimerized with Bcl-2. Mcl-1 also heterodimerized with some Bcl-2 family members like Bok, Bax, Bak and Bik. In this study, I analyzed Mcl-1 function in lymphocyte through searching for its interaction proteins by the yeast two hybrid system. By screening the human lymphocyte library, I found 58 candidates that may interact with Mcl-1, including Bax, Bid and Bik that belong to the Bcl-2 family. I also found some unidentified human genes named KIAA0147, KIAA0719, and one tumor protein, named TPT1 (tumor protein, translationally-controlled 1), to interact with Mcl-1 in the yeast two hybrid system. In-vitro GST-pull down assay showed that KIAA0719 and TPT1 but not KIAA0147 interacted with Mcl-1. It remains to be determined whether Mcl-1 interacts with KIAA0719 or with TPT1 in-vivo.
    資料類型: thesis
    顯示於類別:[醫學科學研究所] 博碩士論文

    文件中的檔案:

    檔案 描述 大小格式瀏覽次數
    摘要.doc28KbMicrosoft Word184檢視/開啟
    摘要.pdf61KbAdobe PDF489檢視/開啟
    摘要.ppt121KbMicrosoft Powerpoint227檢視/開啟
    摘要.ps330KbPostscript84檢視/開啟


    在TMUIR中所有的資料項目都受到原著作權保護.

    TAIR相關文章

    著作權聲明 Copyright Notice

    • 本平台之數位內容為臺北醫學大學所收錄之機構典藏，包含體系內各式學術著作及學術產出。秉持開放取用的精神，提供使用者進行資料檢索、下載與取用，惟仍請適度、合理地於合法範圍內使用本平台之內容，以尊重著作權人之權益。商業上之利用，請先取得著作權人之授權。

      The digital content on this platform is part of the Taipei Medical University Institutional Repository, featuring various academic works and outputs from the institution. It offers free access to academic research and public education for non-commercial use. Please use the content appropriately and within legal boundaries to respect copyright owners' rights. For commercial use, please obtain prior authorization from the copyright owner.

    • 瀏覽或使用本平台，視同使用者已完全接受並瞭解聲明中所有規範、中華民國相關法規、一切國際網路規定及使用慣例，並不得為任何不法目的使用TMUIR。

      By utilising the platform, users are deemed to have fully accepted and understood all the regulations set out in the statement, relevant laws of the Republic of China, all international internet regulations, and usage conventions. Furthermore, users must not use TMUIR for any illegal purposes.

    • 本平台盡力防止侵害著作權人之權益。若發現本平台之數位內容有侵害著作權人權益情事者，煩請權利人通知本平台維護人員([email protected])，將立即採取移除該數位著作等補救措施。

      TMUIR is made to protect the interests of copyright owners. If you believe that any material on the website infringes copyright, please contact our staff([email protected]). We will remove the work from the repository.

    Back to Top
    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - 回饋