钙激活氯离子通道与囊性纤维化跨膜传导调节因子之间的相互作用。

Interaction between calcium-activated chloride channels and the cystic fibrosis transmembrane conductance regulator.

作者信息

Wei L, Vankeerberghen A, Cuppens H, Eggermont J, Cassiman J J, Droogmans G, Nilius B

机构信息

Laboratorium voor Fysiologie, KU Leuven, Belgium.

出版信息

Pflugers Arch. 1999 Oct;438(5):635-41. doi: 10.1007/s004249900108.

DOI:10.1007/s004249900108

PMID:10555560

Abstract

We investigated interactions between cystic fibrosis conductance regulator (CFTR) and endogenous Ca2+-activated Cl- channels (CaCC) in bovine pulmonary artery endothelium (CPAE). CPAE cells, which do not express CFTR, were transiently transfected with wild-type (WT) CFTR and the deletion mutant deltaF508 CFTR. Currents through CaCC were significantly reduced after expression of WT CFTR. This inhibition was increased by stimulation (isobutylmethylxanthine, forskolin) of CFTR in cells expressing WT CFTR. There were no such effects when deltaF508 mutant CFTR, which is retained in the endoplasmic reticulum, was expressed. It is concluded that CFTR and CaCC are functionally coupled probably through a direct channel-channel interaction.

摘要

我们研究了牛肺动脉内皮细胞（CPAE）中囊性纤维化跨膜传导调节因子（CFTR）与内源性钙激活氯离子通道（CaCC）之间的相互作用。不表达CFTR的CPAE细胞被野生型（WT）CFTR和缺失突变体ΔF508 CFTR瞬时转染。WT CFTR表达后，通过CaCC的电流显著降低。在表达WT CFTR的细胞中，CFTR的刺激（异丁基甲基黄嘌呤、福斯可林）会增强这种抑制作用。当保留在内质网中的ΔF508突变体CFTR表达时，没有此类效应。结论是CFTR和CaCC可能通过直接的通道-通道相互作用在功能上偶联。