福司可林对电压门控钾通道Kv11和Kv1 4的调节作用

Modulation of voltage-gated K(+) channels Kv11 and Kv1 4 by forskolin.

作者信息

Matthias K, Seifert G, Reinhardt S, Steinhäuser C

机构信息

Experimental Neurobiology, Neurosurgery, University of Bonn, Sigmund-Freud-Str. 25, 53105, Bonn, Germany.

出版信息

Neuropharmacology. 2002 Sep;43(3):444-9. doi: 10.1016/s0028-3908(02)00115-6.

DOI:10.1016/s0028-3908(02)00115-6

PMID:12243774

Abstract

Forskolin (FSK) affects voltage-gated K(+) (Kv) currents in different cell types, but it is not known which of the various subunits form FSK-sensitive Kv channels. We compared the effect of the compound at Kv1.1 and Kv1.4 channels ectopically expressed in HEK 293 cells. Low FSK concentrations induced a phosphorylation-dependent potentiation of Kv1.1 currents. At higher concentrations, this effect was superimposed by a fast, cAMP-independent channel block. Kv1.4 currents were inhibited with lower potency by FSK but were not modified by phosphorylation. The variable effect of the compound might help to distinguish between Kv subunits expressed by native cells.

摘要

福斯高林（FSK）会影响不同细胞类型中的电压门控钾离子（Kv）电流，但尚不清楚各种亚基中哪些构成了对FSK敏感的Kv通道。我们比较了该化合物对在HEK 293细胞中异位表达的Kv1.1和Kv1.4通道的影响。低浓度的FSK会诱导Kv1.1电流发生磷酸化依赖性增强。在较高浓度下，这种效应会被一种快速的、不依赖cAMP的通道阻断所叠加。FSK对Kv1.4电流的抑制作用较弱，且不受磷酸化的影响。该化合物的不同效应可能有助于区分天然细胞表达的Kv亚基。