Zhang Z, Tang Y, Zhu M X
Neurobiotechnology Center and Department of Neuroscience, Ohio State University, 168 Rightmire Hall, 1060 Carmack Road, Columbus, OH 43210, USA.
Biochem J. 2001 Mar 15;354(Pt 3):717-25. doi: 10.1042/0264-6021:3540717.
Drosophila transient receptor potential (Trp) and its mammalian homologues are postulated to form capacitative Ca2+ entry or store-operated channels. Here we show that expression of murine Trp4 in HEK 293 cells also leads to an increase in inwardly rectifying K+ currents. No similar increase was found in cell lines expressing Trp1, Trp3 or Trp6. Consistent with typical characteristics of inward rectifiers, the K+ currents in Trp4-expressing cells were blocked by low millimolar concentrations of Cs+ and Ba2+, but not by 1.2 mM Ca2+, and were only slightly inhibited by 5 mM tetraethylammonium. Single channel recordings of excised inside-out patches revealed the presence of two conducting states of 51 pS and 94 pS in Trp4-expressing cells. The outward current in the excised patches was blocked by 1 mM spermine, but not by 1 mM Mg2+. How Trp4 expression causes the increase in the K+ currents is not known. We propose that Trp4 either participates in the formation of a novel K+ channel or up-regulates the expression or activity of endogenous inwardly rectifying K+ channels.
果蝇瞬时受体电位(Trp)及其哺乳动物同源物被推测可形成容量性Ca2+内流通道或储存-操作性通道。在此我们表明,在HEK 293细胞中表达小鼠Trp4也会导致内向整流钾电流增加。在表达Trp1、Trp3或Trp6的细胞系中未发现类似的增加。与内向整流器的典型特征一致,表达Trp4的细胞中的钾电流被低毫摩尔浓度的Cs+和Ba2+阻断,但不被1.2 mM Ca2+阻断,且仅被5 mM四乙铵轻微抑制。对切除的内面向外膜片进行的单通道记录显示,表达Trp4的细胞中存在51 pS和94 pS两种传导状态。切除的膜片中的外向电流被1 mM精胺阻断,但不被1 mM Mg2+阻断。Trp4表达如何导致钾电流增加尚不清楚。我们提出,Trp4要么参与新型钾通道的形成,要么上调内源性内向整流钾通道的表达或活性。