K(+)-Cl(-)共转运蛋白 3a 的 N 端对于上调 Na(+),K(+)-ATP 酶活性至关重要。
The NH(2)-terminus of K(+)-Cl(-) cotransporter 3a is essential for up-regulation of Na(+),K(+)-ATPase activity.
机构信息
Department of Pharmaceutical Physiology, University of Toyama, Toyama 930-0194, Japan.
出版信息
Biochem Biophys Res Commun. 2010 Sep 3;399(4):683-7. doi: 10.1016/j.bbrc.2010.08.002. Epub 2010 Aug 5.
K(+)-Cl(-) cotransporter-3 has two major amino terminal variants, KCC3a and KCC3b. In LLC-PK1 cells, exogenously expressed KCC3a co-immunoprecipitated with endogenous Na(+),K(+)-ATPase alpha1-subunit (alpha1NaK), accompanying significant increases of the Na(+),K(+)-ATPase activity. Exogenously expressed KCC3b did not co-immunoprecipitate with endogenous alpha1NaK inducing no change of the Na(+),K(+)-ATPase activity. A KCC inhibitor attenuated the Na(+),K(+)-ATPase activity in rat gastric mucosa in which KCC3a is predominantly expressed, while it had no effects on the Na(+),K(+)-ATPase activity in rat kidney in which KCC3b is predominantly expressed. In these tissue samples, KCC3a co-immunoprecipitated with alpha1NaK, while KCC3b did not. Our results suggest that the NH(2)-terminus of KCC3a is a key region for association with alpha1NaK, and that KCC3a but not KCC3b can regulate the Na(+),K(+)-ATPase activity.
K(+) - Cl(-) 协同转运蛋白-3 有两个主要的氨基末端变体，KCC3a 和 KCC3b。在 LLC-PK1 细胞中，外源性表达的 KCC3a 与内源性 Na(+)，K(+)-ATPase alpha1 亚基 (alpha1NaK) 共免疫沉淀，伴随着 Na(+)，K(+)-ATPase 活性的显著增加。外源性表达的 KCC3b 不会与内源性 alpha1NaK 共免疫沉淀，也不会引起 Na(+)，K(+)-ATPase 活性的变化。KCC 抑制剂在 KCC3a 主要表达的大鼠胃黏膜中减弱了 Na(+)，K(+)-ATPase 活性，而在 KCC3b 主要表达的大鼠肾脏中没有影响。在这些组织样本中，KCC3a 与 alpha1NaK 共免疫沉淀，而 KCC3b 则没有。我们的研究结果表明，KCC3a 的氨基末端是与 alpha1NaK 结合的关键区域，并且只有 KCC3a 而不是 KCC3b 可以调节 Na(+)，K(+)-ATPase 活性。
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