ArticleMolecular biology of the cell2003
Intracellular Na+ controls cell surface expression of Na,K-ATPase via a cAMP-independent PKA pathway in mammalian kidney collecting duct cells.
Article in Molecular biology of the cell, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 61 citations in OpenAlex.
- Diseases caused by mutations in the NaAmerican journal of physiology. Cell physiology · 2021Review
- Activation of GPR56, a novel adhesion GPCR, is necessary for nuclear androgen receptor signaling in prostate cells.PloS one · 2020Article
- Chemical genetic identification of GAK substrates reveals its role in regulating NaLife science alliance · 2018Article
- Salt-induced NaPflugers Archiv : European journal of physiology · 2017Article
- Coordinated Control of ENaC and Na+,K+-ATPase in Renal Collecting Duct.Journal of the American Society of Nephrology : JASN · 2016Review
- The mineralocorticoid receptor (MR) regulates ENaC but not NCC in mice with random MR deletion.Pflugers Archiv : European journal of physiology · 2016Article
- Neuronostatin acts via GPR107 to increase cAMP-independent PKA phosphorylation and proglucagon mRNA accumulation in pancreatic α-cells.American journal of physiology. Regulatory, integrative and comparative physiology · 2016Article
- Transcriptional regulators of Na,K-ATPase subunits.Frontiers in cell and developmental biology · 2015Review
- Sodium transport is modulated by p38 kinase-dependent cross-talk between ENaC and Na,K-ATPase in collecting duct principal cells.Journal of the American Society of Nephrology : JASN · 2014Article
- Article
- Angiotensin II-induced hypertension increases plasma membrane Na pump activity by enhancing Na entry in rat thick ascending limbs.American journal of physiology. Renal physiology · 2013Article
- Protein kinase A (PKA) phosphorylation of Na+/K+-ATPase opens intracellular C-terminal water pathway leading to third Na+-binding site in molecular dynamics simulations.The Journal of biological chemistry · 2012Article
- Rab11b regulates the trafficking and recycling of the epithelial sodium channel (ENaC).American journal of physiology. Renal physiology · 2012Article
- Amphotericin B membrane action: role for two types of ion channels in eliciting cell survival and lethal effects.The Journal of membrane biology · 2010Review
- AS160 modulates aldosterone-stimulated epithelial sodium channel forward trafficking.Molecular biology of the cell · 2010Article
- Protein kinase A activation confers resistance to trastuzumab in human breast cancer cell lines.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009Article
- Proteinase-activated receptor 2 stimulates Na,K-ATPase and sodium reabsorption in native kidney epithelium.The Journal of biological chemistry · 2008Article
- An obligatory heterodimer of 14-3-3beta and 14-3-3epsilon is required for aldosterone regulation of the epithelial sodium channel.The Journal of biological chemistry · 2008Article
- Trafficking of Na-K-ATPase and dopamine receptor molecules induced by changes in intracellular sodium concentration of renal epithelial cells.American journal of physiology. Renal physiology · 2008Article
- Androgens transduce the G alphas-mediated activation of protein kinase A in prostate cells.Cancer research · 2008Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the mammalian kidney the fine control of Na+ reabsorption takes place in collecting duct principal cells where basolateral Na,K-ATPase provides the driving force for vectorial Na+ transport. In the cortical collecting duct (CCD), a rise in intracellular Na+ concentration ([Na+]i) was shown to increase Na,K-ATPase activity and the number of ouabain binding sites, but the mechanism responsible for this event has not yet been elucidated. A rise in [Na+]i caused by incubation with the Na+ ionophore nystatin, increased Na,K-ATPase activity and cell surface expression to the same extent in isolated rat CCD. In cultured mouse mpkCCDcl4 collecting duct cells, increasing [Na+]i either by cell membrane permeabilization with amphotericin B or nystatin, or by incubating cells in a K(+)-free medium, also increased Na,K-ATPase cell surface expression. The [Na+]i-dependent increase in Na,K-ATPase cell-surface expression was prevented by PKA inhibitors H89 and PKI. Moreover, the effects of [Na+]i and cAMP were not additive. However, [Na+]i-dependent activation of PKA was not associated with an increase in cellular cAMP but was prevented by inhibiting the proteasome. These findings suggest that Na,K-ATPase may be recruited to the cell membrane following an increase in [Na+]i through cAMP-independent PKA activation that is itself dependent on proteasomal activity.
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