Suppr超能文献

PI(4,5)P2 对电压门控钾通道的调节作用。

Regulation of voltage-gated potassium channels by PI(4,5)P2.

机构信息

Department of Physiology and Biophysics, University of Washington, Seattle, WA 98195, USA.

出版信息

J Gen Physiol. 2012 Aug;140(2):189-205. doi: 10.1085/jgp.201210806.

Abstract

Phosphatidylinositol 4,5-bisphosphate (PI(4,5)P(2)) regulates activities of numerous ion channels including inwardly rectifying potassium (K(ir)) channels, KCNQ, TRP, and voltage-gated calcium channels. Several studies suggest that voltage-gated potassium (K(V)) channels might be regulated by PI(4,5)P(2). Wide expression of K(V) channels in different cells suggests that such regulation could have broad physiological consequences. To study regulation of K(V) channels by PI(4,5)P(2), we have coexpressed several of them in tsA-201 cells with a G protein-coupled receptor (M(1)R), a voltage-sensitive lipid 5-phosphatase (Dr-VSP), or an engineered fusion protein carrying both lipid 4-phosphatase and 5-phosphatase activity (pseudojanin). These tools deplete PI(4,5)P(2) with application of muscarinic agonists, depolarization, or rapamycin, respectively. PI(4,5)P(2) at the plasma membrane was monitored by Förster resonance energy transfer (FRET) from PH probes of PLCδ1 simultaneously with whole-cell recordings. Activation of Dr-VSP or recruitment of pseudojanin inhibited K(V)7.1, K(V)7.2/7.3, and K(ir)2.1 channel current by 90-95%. Activation of M(1)R inhibited K(V)7.2/7.3 current similarly. With these tools, we tested for potential PI(4,5)P(2) regulation of activity of K(V)1.1/K(V)β1.1, K(V)1.3, K(V)1.4, and K(V)1.5/K(V)β1.3, K(V)2.1, K(V)3.4, K(V)4.2, K(V)4.3 (with different KChIPs and DPP6-s), and hERG/KCNE2. Interestingly, we found a substantial removal of inactivation for K(V)1.1/K(V)β1.1 and K(V)3.4, resulting in up-regulation of current density upon activation of M(1)R but no changes in activity upon activating only VSP or pseudojanin. The other channels tested except possibly hERG showed no alteration in activity in any of the assays we used. In conclusion, a depletion of PI(4,5)P(2) at the plasma membrane by enzymes does not seem to influence activity of most tested K(V) channels, whereas it does strongly inhibit members of the K(V)7 and K(ir) families.

摘要

磷脂酰肌醇 4,5-二磷酸(PI(4,5)P(2))调节许多离子通道的活性,包括内向整流钾(K(ir))通道、KCNQ、TRP 和电压门控钙通道。几项研究表明,电压门控钾(K(V))通道可能受 PI(4,5)P(2)调节。不同细胞中广泛表达的 K(V)通道表明,这种调节可能具有广泛的生理后果。为了研究 PI(4,5)P(2)对 K(V)通道的调节作用,我们在 tsA-201 细胞中与 G 蛋白偶联受体(M(1)R)、电压敏感脂质 5-磷酸酶(Dr-VSP)或携带脂质 4-磷酸酶和 5-磷酸酶活性的工程融合蛋白(pseudojanin)共表达了几种 K(V)通道。这些工具分别通过应用毒蕈碱激动剂、去极化或雷帕霉素来消耗 PI(4,5)P(2)。通过 PLCδ1 的 PH 探针从Förster 共振能量转移(FRET)监测质膜上的 PI(4,5)P(2),同时进行全细胞记录。Dr-VSP 的激活或 pseudojanin 的募集抑制 K(V)7.1、K(V)7.2/7.3 和 K(ir)2.1 通道电流 90-95%。M(1)R 的激活也抑制了 K(V)7.2/7.3 电流。使用这些工具,我们测试了 PI(4,5)P(2)对 K(V)1.1/K(V)β1.1、K(V)1.3、K(V)1.4 和 K(V)1.5/K(V)β1.3、K(V)2.1、K(V)3.4、K(V)4.2、K(V)4.3(与不同的 KChIPs 和 DPP6-s)和 hERG/KCNE2 的潜在调节作用。有趣的是,我们发现 K(V)1.1/K(V)β1.1 和 K(V)3.4 的失活大量去除,导致 M(1)R 激活时电流密度增加,但仅激活 VSP 或 pseudojanin 时没有活性变化。在我们使用的所有测定中,除 hERG 外,其他测试的通道似乎都没有改变活性。总之,质膜上 PI(4,5)P(2)的消耗似乎不会影响大多数测试的 K(V)通道的活性,而强烈抑制 K(V)7 和 K(ir)家族的成员。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6de1/3409096/a69e88be4a7d/JGP_201210806_Fig1.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验