ArticleCellular signalling2015
Renal proximal tubule Na,K-ATPase is controlled by CREB-regulated transcriptional coactivators as well as salt-inducible kinase 1.
Article in Cellular signalling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- The Human PNPLA3FASEB bioAdvances · 2026Article
- Molecular Basis of Na, K-ATPase Regulation of Diseases: Hormone and FXYD2 Interactions.International journal of molecular sciences · 2024Review
- Understanding the roles of salt-inducible kinases in cardiometabolic disease.Frontiers in physiology · 2024Review
- The Triad NaInternational journal of molecular sciences · 2023Article
- Renal oncometabolite L-2-hydroxyglutarate imposes a block in kidney tubulogenesis: Evidence for an epigenetic basis for the L-2HG-induced impairment of differentiation.Frontiers in endocrinology · 2022Article
- Activation of Crtc2/Creb1 in skeletal muscle enhances weight loss during intermittent fasting.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Kidney dopamine DAmerican journal of physiology. Renal physiology · 2019Article
- Salt Inducible Kinase Signaling Networks: Implications for Acute Kidney Injury and Therapeutic Potential.International journal of molecular sciences · 2019Review
- MiR-192-5p in the Kidney Protects Against the Development of Hypertension.Hypertension (Dallas, Tex. : 1979) · 2019Article
- Gene Level Regulation of Na,K-ATPase in the Renal Proximal Tubule Is Controlled by Two Independent but Interacting Regulatory Mechanisms Involving Salt Inducible Kinase 1 and CREB-Regulated Transcriptional Coactivators.International journal of molecular sciences · 2018Review
- Analysing the Expression of Eight Clock Genes in Five Tissues From Fasting and Fed Sows.Frontiers in genetics · 2018Article
- Data on Na,K-ATPase in primary cultures of renal proximal tubule cells treated with catecholamines.Data in brief · 2016Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Sodium reabsorption by the kidney is regulated by locally produced natriuretic and anti-natriuretic factors, including dopamine and norepinephrine, respectively. Previous studies indicated that signaling events initiated by these natriuretic and anti-natriuretic factors achieve their effects by altering the phosphorylation of Na,K-ATPase in the renal proximal tubule, and that protein kinase A (PKA) and calcium-mediated signaling pathways are involved. The same signaling pathways also control the transcription of the Na,K-ATPase β subunit gene atp1b1 in renal proximal tubule cells. In this report, evidence is presented that (1) both the recently discovered cAMP-regulated transcriptional coactivators (CRTCs) and salt-inducible kinase 1 (SIK1) contribute to the transcriptional regulation of atp1b1 in renal proximal tubule (RPT) cells and (2) renal effectors, including norepinephrine, dopamine, prostaglandins, and sodium, play a role. Exogenously expressed CRTCs stimulate atp1b1 transcription. Evidence for a role of endogenous CRTCs includes the loss of transcriptional regulation of atp1b1 by a dominant-negative CRTC, as well as by a CREB mutant, with an altered CRTC binding site. In a number of experimental systems, SIK phosphorylates CRTCs, which are then sequestered in the cytoplasm, preventing their nuclear effects. Consistent with such a role of SIK in primary RPT cells, atp1b1 transcription increased in the presence of a dominant-negative SIK1, and in addition, regulation by dopamine, norepinephrine, and monensin was disrupted by a dominant-negative SIK1. These latter observations can be explained if SIK1 is phosphorylated and inactivated in the presence of these renal effectors. Our results support the hypothesis that Na,K-ATPase in the renal proximal tubule is regulated at the transcriptional level via SIK1 and CRTCs by renal effectors, in addition to the previously reported control of the phosphorylation of Na,K-ATPase.
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