ArticleMolecular biology of the cell1998
Ras pathway activates epithelial Na+ channel and decreases its surface expression in Xenopus oocytes.
Article in Molecular biology of the cell, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 83 citations in OpenAlex.
- Aldosterone: Renal Action and Physiological Effects.Comprehensive Physiology · 2023Article
- Gitelman's Syndrome: characterization of a novel c.1181G>A point mutation and functional classification of the known mutations.Hypertension research : official journal of the Japanese Society of Hypertension · 2018Article
- RhoA increases ASIC1a plasma membrane localization and calcium influx in pulmonary arterial smooth muscle cells following chronic hypoxia.American journal of physiology. Cell physiology · 2018Article
- Regulation of αENaC transcription.Vitamins and hormones · 2015Review
- Role of ASIC1 in the development of chronic hypoxia-induced pulmonary hypertension.American journal of physiology. Heart and circulatory physiology · 2014Article
- Epidermal growth factor-mediated proliferation and sodium transport in normal and PKD epithelial cells.Biochimica et biophysica acta · 2011Review
- A comprehensive analysis of gene expression profiles in distal parts of the mouse renal tubule.Pflugers Archiv : European journal of physiology · 2010Review
- Regulation of renal sodium handling through the interaction between serine proteases and serine protease inhibitors.Clinical and experimental nephrology · 2010Review
- Intact cytoskeleton is required for small G protein dependent activation of the epithelial Na+ channel.PloS one · 2010Article
- AF17 competes with AF9 for binding to Dot1a to up-regulate transcription of epithelial Na+ channel alpha.The Journal of biological chemistry · 2009Article
- Regulated sodium transport in the renal connecting tubule (CNT) via the epithelial sodium channel (ENaC).Pflugers Archiv : European journal of physiology · 2009Review
- Aldosterone responsiveness of the epithelial sodium channel (ENaC) in colon is increased in a mouse model for Liddle's syndrome.The Journal of physiology · 2008Article
- Expression of androgen receptor and androgen regulation of NDRG2 in the rat renal collecting duct.Pflugers Archiv : European journal of physiology · 2005Article
- SGK1 increases Na,K-ATP cell-surface expression and function in Xenopus laevis oocytes.Pflugers Archiv : European journal of physiology · 2004Article
- Regulation of the epithelial sodium channel by accessory proteins.The Biochemical journal · 2003Review
- Activation of mitogen-activated protein kinase (mitogen-activated protein kinase/extracellular signal-regulated kinase) cascade by aldosterone.Molecular biology of the cell · 2002Article
- Effects of aldosterone on biosynthesis, traffic, and functional expression of epithelial sodium channels in A6 cells.The Journal of general physiology · 2002Article
- An improved method for real-time monitoring of membrane capacitance in Xenopus laevis oocytes.Biophysical journal · 2002Article
- Epithelial sodium channel regulated by aldosterone-induced protein sgk.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
- Defective regulation of the epithelial Na+ channel by Nedd4 in Liddle's syndrome.The Journal of clinical investigation · 1999Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The small G protein K-Ras2A is rapidly induced by aldosterone in A6 epithelia. In these Xenopus sodium reabsorbing cells, aldosterone rapidly activates preexisting epithelial Na+ channels (XENaC) via a transcriptionally mediated mechanism. In the Xenopus oocytes expression system, we tested whether the K-Ras2A pathway impacts on XENaC activity by expressing XENaC alone or together with XK-Ras2A rendered constitutively active (XK-Ras2AG12V). As a second control, XENaC-expressing oocytes were treated with progesterone, a sex steroid that induces maturation of the oocytes similarly to activated Ras. Progesterone or XK-Ras2AG12V led to oocyte maturation characterized by a decrease in surface area and endogenous Na+ pump function. In both conditions, the surface expression of exogenous XENaC's was also decreased; however, in comparison with progesterone-treated oocytes, XK-ras2AG12V-coinjected oocytes expressed a fivefold higher XENaC-mediated macroscopic Na+ current that was as high as that of control oocytes. Thus, the Na+ current per surface-expressed XENaC was increased by XK-Ras2AG12V. The chemical driving force for Na+ influx was not changed, suggesting that XK-Ras2AG12V increased the mean activity of XENaCs at the oocyte surface. These observations raise the possibility that XK-Ras2A, which is the first regulatory protein known to be transcriptionally induced by aldosterone, could play a role in the control of XENaC function in aldosterone target cells.
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