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首页> 外文期刊>American Journal of Physiology >FXYD proteins: new regulators of Na-K-ATPase.
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FXYD proteins: new regulators of Na-K-ATPase.

机译：FXYD蛋白：Na-K-ATPase的新调节剂。

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摘要

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 therole of FXYD proteins in the modulation of Na-K-ATPase as well as of other proteins, their regulation, and their structure-function relationship.
机译：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是FXYD1（磷脂酶），FXYD2（Na-K​​-ATPase的γ-亚基），FXYD3（Mat-8），FXYD4（CHIF）和FXYD7。 Na-K-ATPase的辅助亚基，并以组织和异构体特异性方式调节Na-K-ATPase的活性。这些结果强调了通过Na-K-ATPase调节Na +和K +处理的复杂性，这对于确保适当的组织功能（例如肾脏对Na +的重吸收，肌肉收缩性和神经元兴奋性）是必不可少的。此外，FXYD2的突变与人类低镁血症有关，这表明FXYD蛋白对Na-K-ATPase的调节扰动可能与病理生理状态密切相关。更好地了解这种新型的Na-K-ATPase调控机制，应有助于进一步了解其在病理生理状态中的作用。这篇综述总结了有关FXYD蛋白在Na-K-ATPase以及其他蛋白的调节中的作用的现有知识，它们的调控及其结构-功能关系。

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