ASIA unversity:Item 310904400/8769
English  |  正體中文  |  简体中文  |  全文笔数/总笔数 : 90570/105786 (86%)
造访人次 : 16370103      在线人数 : 299
RC Version 6.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
搜寻范围 查询小技巧:
  • 您可在西文检索词汇前后加上"双引号",以获取较精准的检索结果
  • 若欲以作者姓名搜寻,建议至进阶搜寻限定作者字段,可获得较完整数据
  • 进阶搜寻


    题名: Drug design for XRCC4 in silico
    作者: uang, Hung-Jin;Tsai, Fuu-Jen;Chung, Jing-Gung;Tsai, Chang-Hai;Hsu, Yuan-Man;Ho, Tin-Yun;Chang, Yea-Huey;Bau, Da-Tian;Tsai, Ming-Hsui;Chen, Calvin Yu-Chian
    贡献者: Department of Bioinformatics
    关键词: Binding energy;DNA;Docking;Genes;Anticancer drug;Cancer cells;Complex formations;DNA ligases;DNA repair;Drug Design;In-silico;Inhibitory effect;Nonhomologous end joining;Oral cancer;Potent compounds;Structure-based drug design;Traditional Chinese Medicine
    日期: 2009
    上传时间: 2010-04-08 20:05:54 (UTC+8)
    出版者: Asia University
    摘要: XRCC4-DNA ligase IV complex is critical in non-homologous end-joining DNA repair system. Inhibition of its formation is potential in cancer cell killing, while no related study was reported. Herein, the structure-based drug design was used to develop potent compounds in this study. Firstly, the Traditional Chinese Medicine database was employed to dock into the binding site of XRCC4; then the top 10 output compounds were regarded as the scaffolds for further de novo evolution. Secondly, 99 diversities outcome were screened by Lipinski's Rule (rules of five) and the survivors were put into the second round of docking study. As a result, diversities with higher DockScore than the top 10 of DockScore from the first round were selected for pose analysis. Finally, 8 diversities were suggested to behave strongest inhibitory effects on XRCC4-DNA ligase IV complex formation. The 8 candidates selected by this study may serve as potent personalized anticancer drugs. ©2009 IEEE.
    關聯: Proceedings of the 2009 2nd International Conference on Biomedical Engineering and Informatics, BMEI 2009
    显示于类别:[生物資訊與醫學工程學系 ] 會議論文


    档案 描述 大小格式浏览次数
    310904400-8769.doc44KbMicrosoft Word403检视/开启


    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - 回馈