Identification of a pool of non-pumping Na/K-ATPase
Identification of a pool of non-pumping Na/K-ATPase
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DOI：
10.1074/jbc.m609181200
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发表时间：
2007-04-06
影响因子：
4.8
通讯作者：
Xie, Zi-Jian
中科院分区：
文献类型：
--
作者：
Liang, Man;Tian, Jiang;Xie, Zi-Jian
最近的研究将许多非泵功能归因于Na/K-ATPase。在这里，我们提出的实验证据表明，在LLC-PK1细胞中，超过一半的质膜Na/K-ATPase正在执行离子泵以外的细胞功能。这个“非泵送”的Na/K-ATPase池，就像抽水泵一样，与哇巴因结合。胆固醇或小窝蛋白-1的耗尽使一些“非泵送”的Na/K-ATPase进入泵池。Na/K-ATPaseα1亚基的分级敲除最终导致在保留抽水池的同时失去这个“非抽水池”。我们先前的研究表明，非泵浦池的丧失与受体功能的丧失有关，哇巴因给药未能诱导Src和/或ERK的激活就是明证。因此，我们的新发现表明，至少在某些类型的细胞中，大量的表面表达的Na/K-ATPase可能作为非规范的哇巴因结合受体发挥作用。
Recent studies have ascribed many non-pumping functions to the Na/K-ATPase. Here, we present experimental evidence demonstrating that over half of the plasma membrane Na/K-ATPase in LLC-PK1 cells is performing cellular functions other than ion pumping. This "non-pumping" pool of Na/K-ATPase, like the pumping pump, binds ouabain. Depletion of either cholesterol or caveolin-1 moves some of the "non-pumping" Na/K-ATPase into the pumping pool. Graded knock-down of the alpha 1 subunit of the Na/K-ATPase eventually results in loss of this "non-pumping" pool while preserving the pumping pool. Our prior studies indicate that a loss of the non-pumping pool is associated with a loss of receptor function as evidenced by the failure of ouabain administration to induce the activation of Src and/or ERK. Therefore, our new findings suggest that a substantial amount of surface-expressed Na/K-ATPase, at least in some types of cells, may function as non-canonical ouabain-binding receptors.