Geering Käthi
Dept. of Pharmacology and Toxicology, Univ. of Lausanne, Rue du Bugnon 27, 1005 Lausanne, Switzerland.
Am J Physiol Renal Physiol. 2006 Feb;290(2):F241-50. doi: 10.1152/ajprenal.00126.2005.
FXYD proteins belong to a family of small-membrane proteins. Recent experimental evidence suggests that at least five of the seven members of this family, FXYD1 (phospholemman), FXYD2 (gamma-subunit of Na-K-ATPase), FXYD3 (Mat-8), FXYD4 (CHIF), and FXYD7, are auxiliary subunits of Na-K-ATPase and regulate Na-K-ATPase activity in a tissue- and isoform-specific way. These results highlight the complexity of the regulation of Na+ and K+ handling by Na-K-ATPase, which is necessary to ensure appropriate tissue functions such as renal Na+ reabsorption, muscle contractility, and neuronal excitability. Moreover, a mutation in FXYD2 has been linked to cases of human hypomagnesemia, indicating that perturbations in the regulation of Na-K-ATPase by FXYD proteins may be critically involved in pathophysiological states. A better understanding of this novel regulatory mechanism of Na-K-ATPase should help in learning more about its role in pathophysiological states. This review summarizes the present knowledge of the role of FXYD proteins in the modulation of Na-K-ATPase as well as of other proteins, their regulation, and their structure-function relationship.
FXYD蛋白属于小膜蛋白家族。最近的实验证据表明,该家族七个成员中的至少五个,即FXYD1(磷膜蛋白)、FXYD2(钠钾ATP酶的γ亚基)、FXYD3(Mat-8)、FXYD4(CHIF)和FXYD7,是钠钾ATP酶的辅助亚基,并以组织和亚型特异性的方式调节钠钾ATP酶的活性。这些结果突出了钠钾ATP酶对钠和钾处理调节的复杂性,这对于确保适当的组织功能(如肾脏钠重吸收、肌肉收缩力和神经元兴奋性)是必要的。此外,FXYD2的突变与人类低镁血症病例有关,表明FXYD蛋白对钠钾ATP酶调节的扰动可能严重参与病理生理状态。更好地理解钠钾ATP酶的这种新型调节机制应有助于更多地了解其在病理生理状态中的作用。本综述总结了目前关于FXYD蛋白在调节钠钾ATP酶以及其他蛋白中的作用、它们的调节及其结构-功能关系的知识。