Regulation of the epithelial sodium channel (ENaC) by membrane trafficking.
Regulation of the epithelial sodium channel (ENaC) by membrane trafficking.
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DOI：
10.1016/j.bbadis.2010.03.010
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发表时间：
2010-12
影响因子：
6.2
通讯作者：
Butterworth, Michael B.
中科院分区：
文献类型：
--
作者：
Butterworth, Michael B.
上皮Na+通道(ENaC)是许多上皮组织重吸收盐分和水分的主要调节因子。ENaC功能异常与几种人类疾病状态直接相关，包括利德尔综合征、假性醛固酮减少症和囊性纤维化，并可能与盐敏感型高血压有关。上皮细胞的ENAC活性受开放概率和通道数目的调节。本文就ENaC在肾皮质集合管细胞内转运和再循环的调控作一综述。ENaC的转运是在更广泛的上皮细胞囊泡转运的背景下讨论的。讨论了利用上皮模型细胞阐明的具有良好特征的通路和蛋白质相互作用，并强调了已知的与ENaC调节的重叠。在跟踪ENaC在CCD上皮细胞中的生命过程中，将讨论通道的根尖递送、内化、再循环和破坏。虽然目前提出的一些途径仍需要与ENaC调节联系起来，ENaC贩运的调节的许多细节仍有待阐明，但对这些机制的了解可能会进一步深入了解ENaC在正常和疾病状态下的活动。
The epithelial Na+ channel (ENaC) is a major regulator of salt and water reabsorption in a number of epithelial tissues. Abnormalities in ENaC function have been directly linked to several human disease states including Liddle syndrome, psuedohypoaldosteronism and cystic fibrosis, and may be implicated in salt-sensitive hypertension. ENaC activity in epithelial cells is regulated both by open probability and channel number. This review focuses on the regulation of ENaC in the cells of the kidney cortical collecting duct by trafficking and recycling. The trafficking of ENaC is discussed in the broader context of epithelial cell vesicle trafficking. Well characterized pathways and protein interactions elucidated using epithelial model cells are discussed and the known overlap with ENaC regulation is highlighted. In following the life of ENaC in CCD epithelial cells the apical delivery, internalization, recycling and destruction of the channel will be discussed. While a number of pathways presented still need to be linked to ENaC regulation and many details of the regulation of ENaC trafficking remain to be elucidated, knowledge of these mechanisms may provide further insights into ENaC activity in normal and disease states.
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影响因子：
4.8
作者：
Butterworth, Michael B.;Edinger, Robert S.;Frizzell, Raymond A.
通讯作者：
Frizzell, Raymond A.
DOI：
10.1152/ajplung.00435.2004
发表时间：
2005-05-01
影响因子：
4.9
作者：
Caldwell, RA;Boucher, RC;Stutts, MJ
通讯作者：
Stutts, MJ
影响因子：
5.5
作者：
Caldwell, RA;Boucher, RC;Stutts, MJ
通讯作者：
Stutts, MJ
影响因子：
5.5
作者：
Balut, C;Steels, P;Jans, D
通讯作者：
Jans, D
影响因子：
168.9
作者：
Baker, EH;Dong, YB;MacGregor, GA
通讯作者：
MacGregor, GA