首页> 外文期刊>Diabetes >Rapid Publication: ATP~4-Mediates Closure of Pancreatic β-Cell ATP-Sensitive Potassium Channels by Interaction With 1 of 4 Identical Sties
【24h】

Rapid Publication: ATP~4-Mediates Closure of Pancreatic β-Cell ATP-Sensitive Potassium Channels by Interaction With 1 of 4 Identical Sties

机译:快速发布:ATP〜4通过与4个相同结点之一的相互作用介导胰腺β细胞ATP敏感性钾通道的关闭

获取原文
获取原文并翻译 | 示例
       

摘要

In pancreatic β-cells, cytosoli [ATP~4-] critically controls insulin secretion via inhibition of ATP-sensitive potas- sium (K_ATP) channels. These channels are heteromulti- mers composed with a 4:4 stoichiometry of an inwardly rectifying K~+ channel subunit (Kir6.2) ;lus a regulatory sulfonylurea receptor. To elucidate stoichiometry of ATP~4- action, we analyzed ATP~4- sensitivity of channels Coassembled form wild-type Kir6.2 and a loss of ATP~4- Sensitivity mutant (G334D).
机译:在胰腺β细胞中,胞质[ATP〜4-]通过抑制ATP敏感性钾(K_ATP)通道来严格控制胰岛素分泌。这些通道是异源多聚体,由内向整流的K +通道亚基(Kir6.2)的化学计量比为4:4;具有调节性磺酰脲受体。为了阐明ATP〜4-作用的化学计量,我们分析了野生型Kir6.2共装配的通道的ATP〜4-敏感性以及ATP〜4-敏感性突变体(G334D)的丧失。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号