Expression of chloride channel, ClC-5, and its role in receptor-mediated endocytosis of albumin in OK cells.
Expression of chloride channel, ClC-5, and its role in receptor-mediated endocytosis of albumin in OK cells.
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OK 细胞中氯离子通道 ClC-5 的表达及其在受体介导的白蛋白内吞作用中的作用。
DOI：
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发表时间：
2001
期刊：
影响因子：
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通讯作者：
M. Takano
中科院分区：
文献类型：
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作者：
Y. Sasaki;J. Nagai;Y. Kitahara;N. Takai;T. Murakami;M. Takano
通过使用蛋白质印迹和 RT-PCR 分析，在 OK 细胞中检测到电压门控氯离子通道 ClC 家族成员 ClC-5 的表达及其 mRNA。在 OK 细胞中检查了氯离子通道抑制剂对受体介导的白蛋白内吞作用的影响，并与液泡 H(+)-ATPase 抑制剂进行了比较。荧光素-异硫氰酸酯 (FITC)-白蛋白（一种受体介导的内吞作用标记物）的积累受到氯离子通道抑制剂 5-硝基-2-(3-苯基丙氨基)-苯甲酸 (NPPB) 的抑制，且呈浓度依赖性。相反，FITC-菊粉（一种液相内吞作用标记物）的摄取不受 NPPB 的影响。其他氯离子通道抑制剂，4,4'-二异硫氰酸二苯乙烯-2-2'-二磺酸和二苯胺-2-羧酸，也抑制 FITC-白蛋白的摄取。 NPPB 以及液泡 H(+)-ATP 酶抑制剂巴弗洛霉素 A(1) 会导致 FITC-白蛋白摄取的亲和力和最大速度降低。这些结果表明，氯离子通道（很可能是 ClC-5）在 OK 细胞中受体介导的白蛋白内吞作用中发挥着重要作用。
By using Western blot and RT-PCR analyses, the expression of ClC-5, a member of the ClC family of voltage-gated chloride channels, and its mRNA was detected in OK cells. The effect of chloride channel inhibitors on receptor-mediated endocytosis of albumin was examined in OK cells and compared to that of vacuolar H(+)-ATPase inhibitors. Accumulation of fluorescein-isothiocyanate (FITC)-albumin, a receptor-mediated endocytosis marker, was inhibited by 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB), a chloride channel inhibitor, in a concentration-dependent fashion. In contrast, uptake of FITC-inulin, a fluid-phase endocytosis marker, was not affected by NPPB. Other chloride channel inhibitors, 4,4'-diisothiocyanatostilbene-2-2'-disulfonic acid and diphenylamine-2-carboxylic acid, also inhibited FITC-albumin uptake. NPPB, as well as a vacuolar H(+)-ATPase inhibitor bafilomycin A(1), caused a decrease in the affinity and in the maximal velocity of FITC-albumin uptake. These results suggest that chloride channel, most likely ClC-5, plays an important role in the receptor-mediated endocytosis of albumin in OK cells.
影响因子：
15.9
作者：
Birn, H;Fyfe, JC;Christensen, EI
通讯作者：
Christensen, EI