English  |  正體中文  |  简体中文  |  全文筆數/總筆數 : 55217/89514 (62%)
造訪人次 : 10718388      線上人數 : 32
RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library & TKU 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://tkuir.lib.tku.edu.tw:8080/dspace/handle/987654321/98561

    題名: Polymorphic Ala-allele carriers at residue 1170 of HER2 associated with Parkinson's disease
    作者: Wang V;Chuang, Tzu-Chao;Kao MC;Shan DE;Soong BW;Shieh TM
    貢獻者: 淡江大學化學學系
    關鍵詞: Parkinson's disease;Polymorphism;Ala carrier;HER2
    日期: 2013-02
    上傳時間: 2014-08-13 12:08:14 (UTC+8)
    出版者: Amsterdam: Elsevier BV
    摘要: Objective
    HER2, a receptor tyrosine kinase, was originally identified based on its role in cancer research. The protein has subsequently received attention for its role in nerve injury and neurodevelopment. We investigated the polymorphic association of HER2 variants at amino acid residues 655 and 1170 with Parkinson's disease (PD), a neurodegenerative disorder.
    Design and methods
    Polymerase chain reaction (PCR) was used to amplify DNA samples from PD patients and control subjects. The resulting PCR fragments, which spanned HER2 residues 655 and 1170, were analyzed by restriction fragment length polymorphism and/or direct nucleotide sequencing.
    The genetic distribution at residue 655 in PD patients did not differ from that in controls. However, homozygosity for genes encoding Pro at residue 1170 (Pro/Pro) occurred at a significantly lower rate among PD subjects. In other words, Ala-allele carries higher frequency in PD, especially among female PD subjects.
    Different signals or potency of the kinase activities resulting from the Ala1170Pro allele of HER2 may be associated with vulnerability to stress on dopaminergic neurons in PD.
    關聯: Journal of the Neurological Sciences 325(1), pp.115-119
    DOI: 10.1016/j.jns.2012.12.017
    顯示於類別:[化學學系暨研究所] 期刊論文


    檔案 描述 大小格式瀏覽次數



    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library & TKU Library IR teams. Copyright ©   - 回饋