Spauschus A, Lentes K U, Wischmeyer E, Dissmann E, Karschin C, Karschin A
Molecular Neurobiology of Signal Transduction, Max Planck Institute for Biophysical Chemistry, Göttingen, Germany.
J Neurosci. 1996 Feb 1;16(3):930-8. doi: 10.1523/JNEUROSCI.16-03-00930.1996.
Transcripts of a gene, GIRK4, that encodes for a 419-amino-acid protein and shows high structural similarity to other subfamily members of G-protein-activated inwardly rectifying K+ channels (GIRK) have been identified in the human hippocampus. When expressed in Xenopus oocytes, GIRK4 yielded functional GIRK channels with activity that was enhanced by the stimulation of coexpressed serotonin 1A receptors. GIRK4 potentiated basal and agonist-induced currents mediated by other GIRK channels, possibly because of channel heteromerization. Despite the structural similarity to a putative rat KATP channel, no ATP sensitivity or KATP-typical pharmacology was observed for GIRK4 alone or GIRK4 transfected in conjunction with other GIRK channels in COS-7 cells. In rat brain, GIRK4 is expressed together with three other subfamily members, GIRK1-3, most likely in identical hippocampal neurons. Thus, heteromerization or an unknown molecular interaction may cause the physiological diversity observed within this class of K+ channels.
已在人类海马体中鉴定出一种基因GIRK4的转录本，该基因编码一种419个氨基酸的蛋白质，与G蛋白激活的内向整流钾通道（GIRK）的其他亚家族成员具有高度的结构相似性。当在非洲爪蟾卵母细胞中表达时，GIRK4产生了功能性GIRK通道，其活性通过共表达的5-羟色胺1A受体的刺激而增强。GIRK4增强了由其他GIRK通道介导的基础电流和激动剂诱导的电流，这可能是由于通道异源二聚化。尽管与假定的大鼠ATP敏感性钾通道在结构上相似，但单独的GIRK4或与其他GIRK通道一起转染到COS-7细胞中的GIRK4均未观察到ATP敏感性或ATP敏感性钾通道典型的药理学特性。在大鼠脑中，GIRK4与其他三个亚家族成员GIRK1-3一起表达，最有可能在相同的海马神经元中。因此，异源二聚化或未知的分子相互作用可能导致在这类钾通道中观察到的生理多样性。
