ArticleAmerican journal of physiology. Renal physiology2012
Protein kinase C-α mediates hypertonicity-stimulated increase in urea transporter phosphorylation in the inner medullary collecting duct.
Article in American journal of physiology. Renal physiology, 2012. 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, 35 citations in OpenAlex.
- Pendrin is upregulated by corticosterone and participates in its pressor response.American journal of physiology. Renal physiology · 2026Article
- Tissue Distribution, Expression and Regulation of Urea Transporters.Sub-cellular biochemistry · 2025Review
- Angiotensin II acts through Rac1 to upregulate pendrin: role of NADPH oxidase.American journal of physiology. Renal physiology · 2024Article
- Pendrin-null mice develop severe hypokalemia following dietary NaAmerican journal of physiology. Renal physiology · 2022Article
- Aldosterone Regulates Pendrin and Epithelial Sodium Channel Activity through Intercalated Cell Mineralocorticoid Receptor-Dependent and -Independent Mechanisms over a Wide Range in Serum Potassium.Journal of the American Society of Nephrology : JASN · 2020Article
- Osmotic regulation of UT-B urea transporters in the RT4 human urothelial cell line.Physiological reports · 2019Article
- Mammalian urine concentration: a review of renal medullary architecture and membrane transporters.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2018Review
- Protein kinase Cα deletion causes hypotension and decreased vascular contractility.Journal of hypertension · 2018Article
- Urea transport and clinical potential of urearetics.Current opinion in nephrology and hypertension · 2016Review
- Hyperosmolality regulates UT-A6 urea transporter expression in the Caco-2 cell line.Physiological reports · 2016Article
- How do kinases contribute to tonicity-dependent regulation of the transcription factor NFAT5?World journal of nephrology · 2016Review
- Activation of protein kinase Cα increases phosphorylation of the UT-A1 urea transporter at serine 494 in the inner medullary collecting duct.American journal of physiology. Cell physiology · 2015Article
- Pendrin localizes to the adrenal medulla and modulates catecholamine release.American journal of physiology. Endocrinology and metabolism · 2015Article
- Urea and Ammonia Metabolism and the Control of Renal Nitrogen Excretion.Clinical journal of the American Society of Nephrology : CJASN · 2015Review
- Activation of protein kinase C-α and Src kinase increases urea transporter A1 α-2, 6 sialylation.Journal of the American Society of Nephrology : JASN · 2015Article
- PKC-α contributes to high NaCl-induced activation of NFAT5 (TonEBP/OREBP) through MAPK ERK1/2.American journal of physiology. Renal physiology · 2015Article
- Role of protein kinase C-α in hypertonicity-stimulated urea permeability in mouse inner medullary collecting ducts.American journal of physiology. Renal physiology · 2013Article
- Molecular mechanisms of urea transport in health and disease.Pflugers Archiv : European journal of physiology · 2012Review
- Lack of protein kinase C-α leads to impaired urine concentrating ability and decreased aquaporin-2 in angiotensin II-induced hypertension.American journal of physiology. Renal physiology · 2012Article
- Urea transporter physiology studied in knockout mice.Frontiers in physiology · 2012Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
The UT-A1 urea transporter plays a critical role in the production of concentrated urine. Both vasopressin and hypertonicity increase urea permeability in rat terminal inner medullary collecting ducts (IMCD). Each agonist independently increases UT-A1 phosphorylation and apical plasma membrane accumulation. Vasopressin activates PKA and phosphorylates UT-A1 at serines 486 and 499. Hypertonicity stimulates urea permeability through protein kinase C (PKC) and intracellular calcium. To determine whether the hypertonic stimulation of urea permeability results from a PKC-mediated phosphorylation of UT-A1, rat IMCDs were metabolically labeled with [(32)P]. Hypertonicity stimulated UT-A1 phosphorylation, and this increase was blocked by preincubation with a PKC inhibitor. IMCDs were biotinylated to assess plasma membrane UT-A1. Hypertonicity increased biotinylated UT-A1, and this increase was blocked by preincubation with a PKC inhibitor. When PKC was directly activated using a phorbol ester, total UT-A1 phosphorylation increased, but phosphorylation at serine 486 was not increased, indicating that PKC did not phosphorylate UT-A1 at the same residue as PKA. Since PKC-α is a calcium-dependent PKC isoform and PKC-α knockout mice have a urine-concentrating defect, it suggested that PKC-α may mediate the response to hypertonicity. Consistent with this hypothesis, hypertonicity increased phospho-PKC-α in rat IMCDs. Finally, PKC-α knockout mice were used to determine whether hypertonicity could stimulate UT-A1 phosphorylation in the absence of PKC-α. Hypertonicity significantly increased UT-A1 phosphorylation in wild-type mice but not in PKC-α knockout mice. We conclude that PKC-α mediates the hypertonicity-stimulated increase in UT-A1 phosphorylation in the IMCD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.