...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Cellular Physiology >ClC-3 is a main component of background chloride channels activated under isotonic conditions by autocrine ATP in nasopharyngeal carcinoma cells.
【24h】

ClC-3 is a main component of background chloride channels activated under isotonic conditions by autocrine ATP in nasopharyngeal carcinoma cells.

机译：氯化ClC-3背景是一个重要组成部分等渗条件下激活渠道在鼻咽癌细胞自分泌ATP。

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

In this study, the activation mechanisms of the background chloride current and the role of the current in maintaining of basal cell volume were investigated in human nasopharyngeal carcinoma CNE-2Z cells. Under isotonic conditions, a background chloride current was recorded by the patch clamp technique. The current presented the properties similar to those of the volume-activated chloride current in the same cell line and was inhibited by chloride channel blockers or by cell shrinkage induced by hypertonic challenges. Extracellular applications of reactive blue 2, a purinergic receptor antagonist, suppressed the background chloride current in a concentration-dependent manner under isotonic conditions. Depletion of extracellular ATP with apyrase or inhibition of ATP release from cells by gadolinium chloride decreased the background current. Extracellular applications of micromolar concentrations of ATP activated a chloride current which was inhibited by chloride channel blockers and hypertonic solutions. Extracellular ATP could also reverse the action of gadolinium chloride. Transfection of CNE-2Z cells with ClC-3 siRNA knocked down expression of ClC-3 proteins, attenuated the background chloride current and prevented activation of the ATP-induced current. Furthermore, knockdown of ClC-3 expression or exposures of cells to ATP (10 mM), the chloride channel blockers 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB) and tamoxifen, or reactive blue 2 increased cell volume under isotonic conditions. The results suggest that ClC-3 protein may be a main component of background chloride channels which can be activated under isotonic conditions by autocrine/paracrine ATP through purinergic receptor pathways; the background current is involved in maintenance of basal cell volume.
机译：在这项研究中,激活的机制氯化背景电流的作用目前在维护的基底细胞体积调查人类鼻咽癌CNE-2Z细胞。当前记录的背景氯膜片钳技术。类似的属性volume-activated氯电流是一样的细胞系,抑制氯通道阻滞剂或细胞收缩引起的高渗性的挑战。purinergic受体活性蓝2拮抗剂,抑制背景氯当前在浓度的方式等渗条件。ATP apyrase或抑制ATP的释放从细胞通过氯化钆下降背景电流。微摩尔的ATP浓度激活氯化氯电流抑制的通道阻滞剂和高渗性的解决方案。细胞外ATP也可以反向操作氯化钆。细胞ClC-3 siRNA可拆卸的表达ClC-3蛋白质,减毒的背景激活的氯电流和预防ATP-induced电流。ClC-3表达式或暴露的细胞ATP (10毫米),氯通道阻滞剂(5-nitro-2) - 3-phenylpropylamino苯甲酸(NPPB)和它莫西芬,或活性蓝2等渗条件下细胞体积增加。结果表明ClC-3蛋白质可能是一个背景氯通道的主要组成部分等渗条件下可以激活通过自分泌/旁分泌通过purinergic ATP受体通路;参与维护基底细胞体积。

著录项

相似文献

  • 外文文献
  • 中文文献
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