Modulation of the Ca2+-activated Cl- channel by 14-3-3ε

被引：22
|
作者：
Chan, HC
Wu, WL
So, SC
Chung, YW
Tsang, LL
Wang, XF
Yan, YC
Luk, SCW
Siu, SS
Tsui, SKW
Fung, KP
Lee, CY
Waye, MMY [1 ]
机构：
[1] Chinese Univ Hong Kong, Hong Kong Bioinformat Ctr, Shatin, Hong Kong, Peoples R China
[2] Chinese Univ Hong Kong, Fac Med, Dept Physiol, Epithelial Cell Biol Res Ctr, Shatin, Hong Kong, Peoples R China
[3] Chinese Univ Hong Kong, Fac Med, Dept Biochem, Shatin, Hong Kong, Peoples R China
[4] Chinese Univ Hong Kong, Chinese Med Mat Res Ctr, Shatin, Hong Kong, Peoples R China
[5] Acad Sinica, Shanghai Inst Cell Biol, Shanghai 200031, Peoples R China
来源：
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2000年 / 270卷 / 02期
基金：
以色列科学基金会;
关键词：
14.3.3; calcium activated chloride channel; calmodulin; Xenopus; human;
D O I：
10.1006/bbrc.2000.2454
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
We have previously reported an association of 14-3-3 epsilon isoform with calmodulin. Using the voltage-clamp technique, the present study investigated the potential role of 14-3-3 in modulating the Ca2+-activated Cl- channel (CaCC) endogenously expressed in Xenopus oocytes. Injection of 14-3-3 epsilon antisense oligodeoxynucleotides resulted in potentiation of the ionomycin-induced Cl- current, while 14-3-3 peptide and calmodulin inhibitor, W13, suppressed the antisense-potentiated current. The data suggest that 14-3-3 epsilon plays an inhibitory role in modulating the CaCC by interacting with the calmodulin-dependent pathway. The potential role of 14-3-3 epsilon in other tissues and its therapeutic potential for cystic fibrosis are discussed. (C) 2000 Academic Press.
引用
收藏
页码：581 / 587
页数：7
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