• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >ATP and PIP2 dependence of the magnesium-inhibited, TRPM7-like cation channel in cardiac myocytes.
【24h】

ATP and PIP2 dependence of the magnesium-inhibited, TRPM7-like cation channel in cardiac myocytes.

机译：心肌细胞中镁抑制的TRPM7样阳离子通道的ATP和PIP2依赖性。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The Mg(2+)-inhibited cation (MIC) current (I(MIC)) in cardiac myocytes biophysically resembles currents of heterologously expressed transient receptor potential (TRP) channels, particularly TRPM6 and TRPM7, known to be important in Mg(2+) homeostasis. To understand the regulation of MIC channels in cardiac cells, we used the whole cell voltage-clamp technique to investigate the role of intracellular ATP in pig, rat, and guinea pig isolated ventricular myocytes. I(MIC), studied in the presence or absence of extracellular divalent cations, was sustained for >or=50 min after patch rupture in ATP-dialyzed cells, whereas in ATP-depleted cells I(MIC) exhibited complete rundown. Equimolar substitution of internal ATP by its nonhydrolyzable analog adenosine 5'-(beta,gamma-imido)triphosphate failed to prevent rundown. In ATP-depleted cells, inhibition of lipid phosphatases by fluoride + vanadate + pyrophosphate prevented I(MIC) rundown. In contrast, under similar conditions neither the inhibition of protein phosphatases 1, 2A, 2B or of protein tyrosine phosphatase nor the activation of protein kinase A (forskolin, 20 microM) or protein kinase C (phorbol myristate acetate, 100 nM) could prevent rundown. In ATP-loaded cells, depletion of phosphatidylinositol 4,5-bisphosphate (PIP(2)) by prevention of its resynthesis (10 microM wortmannin or 15 microM phenylarsine oxide) induced rundown of I(MIC). Finally, loading ATP-depleted cells with exogenous PIP(2) (10 microM) prevented rundown. These results suggest that PIP(2), likely generated by ATP-utilizing lipid kinases, is necessary for maintaining cardiac MIC channel activity.
机译：心肌细胞中的Mg（2+）抑制阳离子（MIC）电流（I（MIC））在生物学上类似于异源表达的瞬时受体电位（TRP）通道，特别是TRPM6和TRPM7的电流，已知在Mg（2+ ）稳态。为了了解心肌细胞中MIC通道的调控，我们使用了全细胞电压钳技术来研究细胞内ATP在猪，大鼠和豚鼠分离的心室肌细胞中的作用。 I（MIC），在有或没有细胞外二价阳离子存在下进行研究，在膜片破裂后在ATP透析的细胞中持续维持> == 50分钟，而在ATP耗尽的细胞中，I（MIC）则显示完全降解。内部ATP被其不可水解的类似物腺苷5'-（β，γ-亚氨基）三磷酸等摩尔取代不能阻止流失。在ATP耗尽的细胞中，氟化物+钒酸盐+焦磷酸盐对脂质磷酸酶的抑制作用可防止I（MIC）减少。相比之下，在类似条件下，蛋白磷酸酶1、2A，2B或蛋白酪氨酸磷酸酶的抑制或蛋白激酶A（福斯高林，20 microM）或蛋白激酶C（佛波肉豆蔻酸酯乙酸盐，100 nM）的激活均不能阻止降解。 。在加载ATP的细胞中，通过阻止磷脂酰肌醇4,5-二磷酸（PIP（2））的再合成（10 microM渥曼青霉素或15 microM苯砷氧化物）而耗尽，导致I（MIC）的流失。最后，用外源PIP（2）（10 microM）加载ATP耗尽的细胞可防止流失。这些结果表明，PIP（2）可能是由利用ATP的脂质激酶产生的，对于维持心脏MIC通道活性是必需的。

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