改变atp敏感性钾通道功能性质赋予小说SUR1的拼接的变体。

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樱花H,特拉普,丽丝B,阿什克罗夫特调频

改变atp敏感性钾通道功能性质赋予小说SUR1的拼接的变体。

杂志。1999年12月1日,Pt 2:337-50 521。

PubMed ID

10581306 (在PubMed

]

文摘

1。ATP-sensitive钾()诱导通道是由造孔(Kir6.x)和监管磺脲受体(SURx)子单元。我们有孤立的小说苏尔变体(SUR1bDelta33)下丘脑cDNA库。这种变体缺乏外显子33和引入了一个转移产生截短蛋白缺乏第二个核苷酸结合域(NBD2)。在下丘脑的低水平表达,分泌细胞中脑、心脏和MIN6胰腺β-细胞线。2。我们检查了atp敏感性钾通道特性由Kir6.2和SUR1bDelta33通过记录宏观电流膜补丁切除从非洲爪蟾蜍卵母细胞表达这些子单元。我们也调查了删除的效果SUR1 (SUR1bT1)开始或结束时(SUR1bT2)外显子33频道诱导特性。3所示。Kir6.2 / SUR1bDelta33显示增强开放概率(Po -60 mV = 0.6),减少ATP敏感性(Ki 86 microM),与野生型相比通道(Po = 0.3; Ki, 22 microM). However, Kir6.2/SUR1bT1 and Kir6.2/SUR1bT2 resembled the wild-type channel in their Po and ATP sensitivity. 4. Neither MgADP, nor the K+ channel opener diazoxide, enhanced Kir6.2/SUR1bDelta33, Kir6.2/SUR1bT1 or Kir6.2/SUR1bT2 currents, consistent with the idea that these agents require an intact NBD2 for their action. Sulphonylureas blocked KATP channels containing any of the three SUR variants, but in excised patches the extent of block was less than that for the wild-type channel. In intact cells, the extent of sulphonylurea block of Kir6.2/SUR1bDelta33 was greater than that in excised patches and was comparable to that found for wild-type channels. 5. Our results demonstrate that NBD2 is not essential for functional expression or sulphonylurea block, but is required for KATP channel activation by K+ channel openers and nucleotides. Some of the unusual properties of Kir6.2/SUR1bDelta33 resemble those reported for the KATP channel of ventromedial hypothalamic (VMH) neurones, but the fact that this mRNA is expressed at low levels in many other tissues makes it less likely that SUR1bDelta33 serves as the SUR subunit for the VMH KATP channel.

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药物靶点

药物	目标	类	生物	药理作用	行动
氯甲苯噻嗪	ATP-sensitive内向整流钾通道11	蛋白质	人类	是的	诱导物	细节