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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >The kinase Grk2 regulates Nedd4/Nedd4-2-dependent control of epithelial Na+ channels.
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The kinase Grk2 regulates Nedd4/Nedd4-2-dependent control of epithelial Na+ channels.

机译：激酶Grk2调节上皮Na +通道的Nedd4 / Nedd4-2依赖性控制。

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摘要

Epithelial Na(+) channels mediate the transport of Na across epithelia in the kidney, gut, and lungs and are required for blood pressure regulation. They are inhibited by ubiquitin protein ligases, such as Nedd4 and Nedd4-2, with loss of this inhibition leading to hypertension. Here, we report that these channels are maintained in the active state by the G protein-coupled receptor kinase, Grk2, which has been previously implicated in the development of essential hypertension. We also show that Grk2 phosphorylates the C terminus of the channel beta subunit and renders the channels insensitive to inhibition by Nedd4-2. This mechanism has not been previously reported to regulate epithelial Na(+) channels and provides a potential explanation for the observed association of Grk2 overactivity with hypertension. Here, we report a G protein-coupled receptor kinase regulating a membrane protein other than a receptor and provide a paradigm for understanding how the interaction between membrane proteins and ubiquitin protein ligases is controlled.
机译：上皮Na（+）通道介导Na跨肾脏，肠和肺上皮细胞的运输，并且是调节血压所必需的。它们受到泛素蛋白连接酶（如Nedd4和Nedd4-2）的抑制，失去这种抑制作用会导致高血压。在这里，我们报道这些通道被G蛋白偶联受体激酶Grk2维持在活跃状态，该激酶先前已参与了原发性高血压的发展。我们还显示，Grk2使通道β亚基的C末端磷酸化，并使通道对Nedd4-2的抑制不敏感。该机制以前尚未报道过调节上皮Na（+）通道，并为观察到的Grk2过度活跃与高血压之间的关联提供了可能的解释。在这里，我们报告一个G蛋白偶联受体激酶调节除受体以外的其他膜蛋白，并为理解膜蛋白和泛素蛋白连接酶之间的相互作用提供了范例。

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