Cell surface expression of the epithelial Na channel and a mutant causing Liddle syndrome: A quantitative approach

Dmitri Firsov; Laurent Schild; Ivan Gautschi

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Cell surface expression of the epithelial Na channel and a mutant causing Liddle syndrome: A quantitative approach

机译：上皮Na通道和引起Liddle综合征的突变体的细胞表面表达：定量方法

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摘要

The epithelial amiloride-sensitive sodium channel (ENaC) controls transepithelial Na~+ movement in Na~+-transporting epithelia and is associated with Liddle syndrome, an autosomal dominant form of salt-sensitive hypertension. Detailed analysis of ENaC channel properties and the functional consequences of mutations causing Liddle syndrome has been, so far, limited by lack of a method allowing specific and quantitative detection of cell-surface- expressed ENaC.

机译：上皮阿米洛利敏感性钠通道（ENaC）控制Na +转运上皮中的上皮Na〜+运动，并与Liddle综合征有关，后者是盐敏感性高血压的常染色体显性形式。迄今为止，对ENaC通道特性和引起Liddle综合征的突变的功能后果的详细分析一直受到缺乏允许对细胞表面表达的ENaC进行特异性和定量检测的方法的限制。

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《Proceedings of the National Academy of Sciences of the United States of America》 |1996年第26期|p.15370-15375|共6页
作者
Dmitri Firsov; Laurent Schild; Ivan Gautschi;
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收录信息美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
原文格式 PDF
正文语种 eng
中图分类自然科学总论;
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1. Epithelial Na+ channel mutants causing Liddle's syndrome retain ability to respond to aldosterone and vasopressin. [J] . Auberson M, Hoffmann-Pochon N, Vandewalle A, American Journal of Physiology . 2003,第3期

机译：引起Liddle综合征的上皮Na +通道突变体保留了对醛固酮和加压素的反应能力。
2. Liddle's syndrome mutations increase Na+ transport through dual effects on epithelial Na+ channel surface expression and proteolytic cleavage [J] . Knight KK, Olson DR, Zhou RF, Proceedings of the National Academy of Sciences of the United States of America . 2006,第8期

机译：Liddle's综合征突变通过对上皮Na +通道表面表达和蛋白水解裂解的双重作用来增加Na +转运
3. A mutation in the epithelial sodium channel causing Liddle disease increases channel activity in the Xenopus laevis oocyte expression system. [J] . Schild L, Canessa CM, Shimkets RA, Proceedings of the National Academy of Sciences of the United States of America . 1995,第12期

机译：导致Liddle病的上皮钠通道中的突变增加了非洲爪蟾卵母细胞表达系统中的通道活性。
4. A Proteome Analysis of AKT1 and Mutant AKT1(E17K) in Human Mammary Epithelial Cells by Mass Spectrometry [C] . Tony Tegeler, Rachelle A. DuQuette, Courtney Van Cott, American Society for Mass Spectrometry Conference on Mass Spectrometry and Allied Topics . 2012

机译：通过质谱法通过乳腺乳腺上皮细胞中Akt1和突变Akt1（E17K）的蛋白质组分析
5. Trafficking and cell surface stability of the epithelial sodium ion channel expressed in epithelial MDCK cells. [D] . Hanwell, David Grant. 2003

机译：在上皮MDCK细胞中表达的上皮钠离子通道的运输和细胞表面稳定性。
6. Cell surface expression of the epithelial Na channel and a mutant causing Liddle syndrome: A quantitative approach [O] . Dmitri Firsov, Laurent Schild, Ivan Gautschi, 1996

机译：上皮Na通道和突变体的细胞表面表达引起里德尔综合症的定量方法
7. Epithelial Na+ channel mutants causing Liddle's syndrome retain ability to respond to aldosterone and vasopressin [O] . Muriel Auberson, Nicole Hoffmann-Pochon, A. Vandewalle, 2003

机译：引起裂片综合征的上皮性Na +通道突变体保留对aldosterone和vasopressin响应的能力
8. Bacillus Anthracis Spores of the bclA Mutant Exhibit Increased Adherence to Epithelial Cells, Fibroblasts, and Endothelial Cells but not to Macrophages [R] . Bozue, J. , Moody, K. L. , Cote, C. K. , 2007

机译：bcla突变体的炭疽芽孢杆菌孢子表现出对上皮细胞，成纤维细胞和内皮细胞的依赖性，但对巨噬细胞没有

Cell surface expression of the epithelial Na channel and a mutant causing Liddle syndrome: A quantitative approach

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