English  |  正體中文  |  简体中文  |  Items with full text/Total items : 28603/40634
Visitors : 4354367      Online Users : 212
RC Version 4.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
Scope Adv. Search

Please use this identifier to cite or link to this item: http://ntour.ntou.edu.tw:8080/ir/handle/987654321/38445

Title: Autoantibodies to dsDNA cross-react with the arginine-glycine-rich domain of heterogeneous nuclear ribonucleoprotein A2 (hnRNP A2) and promote methylation of hnRNP A2.
Authors: Sun KH;Tang SJ;Wang YS;Lin WJ;You RI.
Contributors: 國立臺灣海洋大學:生命科學暨生物科技學系
Date: 2003
Issue Date: 2016-09-01T08:28:34Z
Publisher: Rheumatology(Oxford)
Abstract: Abstract:
This study was designed to clarify the internalization of anti-DNA antibodies (anti-DNA) into living cells in the pathogenesis of systemic lupus erythematosus (SLE) using anti-DNA monoclonal antibodies (mAbs).
Anti-DNA mAbs 9D7, 9D7D2, 9A4, 5E3F5, 12B3H2 and 6E11E3 were prepared by a standard hybridoma procedure to determine the interaction of anti-DNA with proteins in different types of cells.
The anti-DNA mAbs reacted with two protein antigens (35 and 50 kDa) in the cells. The 35-kDa antigen was shown to have 100% homology with hnRNP A2. The arginine-glycine-rich domain in hnRNP A2 was found to be the reaction site, and the methylation of hnRNP A2 by PRMT1 (protein arginine methyltransferase 1) was increased by anti-DNA. Moreover, anti-DNA was demonstrated to bind and internalize into the cytoplasm and nucleus.
Nuclear localizing anti-DNA may cross-react with hnRNP A2 to modulate the inflammatory responses and polarize immune reactions associated with SLE.
Relation: 42(1)
URI: http://ntour.ntou.edu.tw:8080/ir/handle/987654321/38445
Appears in Collections:[生命科學系] 期刊論文

Files in This Item:

File Description SizeFormat

All items in NTOUR are protected by copyright, with all rights reserved.


著作權政策宣告: 本網站之內容為國立臺灣海洋大學所收錄之機構典藏,無償提供學術研究與公眾教育等公益性使用,請合理使用本網站之內容,以尊重著作權人之權益。
網站維護: 海大圖資處 圖書系統組
DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - Feedback