您当前所在位置: 首页 > 学者

 

  • 6浏览

  • 0点赞

  • 0收藏

  • 0分享

  • 13下载

  • 0评论

  • 引用

期刊论文

Activation of G55 1D—CFTR by Bicyclooctane Compounds Is cAM P—dependent and Exhibits Low Sensitivity to Thiaz0lidin0ne CFTR Inhibitor CFTRinh一172

杨红W ANG Ying ZHAO Lu HE Cheng-yan XU Li-na and YANG Hong

CHEM. RES. CHINESE U. 2005, 21 (2), 183-186,-0001,():

URL:

摘要/描述

The G551D-CFTR mutation causing cystic fibrosis(CF)results from a missense mutation at codon 551 (G551D)in the gene encoding of the cystic fibrosis transmembrane conductance regulator(CFTR). The G551D mutation in CFTR results in a reduced functionaI channeI but G551D-CFTR is appropriately inserted in the apicaI membrane. In previous studies we discovered a class of high-affinity bicyclooctane(BC0) G55 1D-CFTR activators(G55 1DBcos)with Kd down to 1mol/L. In this study, we analyzed the pharmaco-Iogical activation of G551D-CFTR by the G551DBcos by means of short circuit current analysis and cell-based fluorescence quenching assay. The G551DBcos-induced G551D-CFTR activation is cAM P-dependent and is Iess sensitive to thiazolidinone CFTR inhibitor CFTRinh-172. These data suggest that(1)the phosphoryla-tion of G551D-CFTR by protein kinase A is required for the activation by G55l[)Bcos;(2)G551DBcoS and CFTRinh-172 may act at the same site on the G551D-CFTR molecule.

【免责声明】以下全部内容由[]上传于[2010年03月08日 15时18分16秒],版权归原创者所有。本文仅代表作者本人观点,与本网站无关。本网站对文中陈述、观点判断保持中立,不对所包含内容的准确性、可靠性或完整性提供任何明示或暗示的保证。请读者仅作参考,并请自行承担全部责任。

我要评论

全部评论 0

本学者其他成果

    同领域成果