ArticleAmerican journal of physiology. Renal physiology2008
Nedd4-2 isoforms ubiquitinate individual epithelial sodium channel subunits and reduce surface expression and function of the epithelial sodium channel.
Article in American journal of physiology. Renal physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Ion channel inhibition by targeted recruitment of NEDD4-2 with divalent nanobodies.Nature communications · 2025Article
- Genetic Modifications to Alter Blood Pressure Level.Biomedicines · 2022Review
- Regulation of epithelial sodium channel activity by SARS-CoV-1 and SARS-CoV-2 proteins.Biophysical journal · 2021Article
- Data integration in physiology using Bayes' rule and minimum Bayes' factors: deubiquitylating enzymes in the renal collecting duct.Physiological genomics · 2017Article
- Nedd4-2 but not Nedd4-1 is critical for protein kinase C-regulated ubiquitination, expression, and transport activity of human organic anion transporter 1.American journal of physiology. Renal physiology · 2016Article
- An Essential Role of Nedd4-2 in the Ubiquitination, Expression, and Function of Organic Anion Transporter-3.Molecular pharmaceutics · 2016Article
- Enhanced expression of epithelial sodium channels causes salt-induced hypertension in mice through inhibition of the α2-isoform of Na+, K+-ATPase.Physiological reports · 2015Article
- Review
- Cholera toxin enhances Na(+) absorption across MCF10A human mammary epithelia.American journal of physiology. Cell physiology · 2014Article
- ENaC activity is increased in isolated, split-open cortical collecting ducts from protein kinase Cα knockout mice.American journal of physiology. Renal physiology · 2014Article
- A regulated NH2-terminal Sgk1 variant with enhanced function is expressed in the collecting duct.American journal of physiology. Renal physiology · 2012Article
- Salt-induced hypertension in a mouse model of Liddle syndrome is mediated by epithelial sodium channels in the brain.Hypertension (Dallas, Tex. : 1979) · 2012Article
- Article
- Respiratory distress and perinatal lethality in Nedd4-2-deficient mice.Nature communications · 2011Article
- Nedd4-2 interacts with occludin to inhibit tight junction formation and enhance paracellular conductance in collecting duct epithelia.American journal of physiology. Renal physiology · 2010Article
- Endothelin-1 inhibits the epithelial Na+ channel through betaPix/14-3-3/Nedd4-2.Journal of the American Society of Nephrology : JASN · 2010Article
- Lysine 63-linked polyubiquitination of the dopamine transporter requires WW3 and WW4 domains of Nedd4-2 and UBE2D ubiquitin-conjugating enzymes.The Journal of biological chemistry · 2010Article
- The activity of the epithelial sodium channels is regulated by caveolin-1 via a Nedd4-2-dependent mechanism.The Journal of biological chemistry · 2009Article
- An evolutionarily conserved N-terminal Sgk1 variant with enhanced stability and improved function.American journal of physiology. Renal physiology · 2008Article
- AICAR activates AMPK and alters PIP2 association with the epithelial sodium channel ENaC to inhibit Na+ transport in H441 lung epithelial cells.The Journal of physiology · 2008Article
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2 authors.
Funding
Abstract
We previously reported the existence of multiple isoforms of human Nedd4-2 (Am J Physiol Renal Physiol 285: F916-F929, 2003). When overexpressed in M-1 collecting duct epithelia, full-length Nedd4-2 (Nedd4-2), Nedd4-2 lacking the NH(2)-terminal C2 domain (Nedd4-2DeltaC2), and Nedd4-2 lacking WW domains 2 and 3 (Nedd4-2DeltaWW2,3) variably reduce benzamil-sensitive Na(+) transport. We investigated the effect of each of the Nedd4-2 isoforms on cell surface expression and ubiquitination of ENaC subunits. We find that alphaENaC when transfected alone or with beta and gammaENaC is expressed at the cell surface and this membrane expression is variably reduced by coexpression with each of the Nedd4-2 isoforms. Nedd4-2 reduces the half-life of ENaC subunits and enhances the ubiquitination of alpha, beta, and gammaENaC subunits when expressed alone or together suggesting that each subunit is a target for Nedd4-2-mediated ubiquitination. As has been reported recently, we confirm that the surface-expressed pool of ENaC is multi-ubiquitinated. Inhibitors of the proteasome increase ubiquitination of ENaC subunits and stimulate Na(+) transport in M-1 cells consistent with a role for the ubiquitin-proteasome pathway in regulating Na(+) transport in the collecting duct.
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