ArticleThe Journal of biological chemistry2010
Glucocorticoid-induced Leucine zipper 1 stimulates the epithelial sodium channel by regulating serum- and glucocorticoid-induced kinase 1 stability and subcellular localization.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 50 citations in OpenAlex.
- SCNN1A expression in triple-negative breast cancer: clinical implications for prognosis and neoadjuvant therapy response.World journal of surgical oncology · 2025Article
- Epithelial NaComprehensive Physiology · 2024Review
- Dietary sodium alters aldosterone's effect on renal sodium transporter expression and distal convoluted tubule remodelling.The Journal of physiology · 2024Article
- Submersion and hypoxia inhibit alveolar epithelial NaRespiratory research · 2023Article
- Aldosterone: Renal Action and Physiological Effects.Comprehensive Physiology · 2023Article
- Noncanonical Form of ERAD Regulates Cardiac Hypertrophy.Circulation · 2023Article
- How Many Cell Types Are in the Kidney and What Do They Do?Annual review of physiology · 2022Review
- Aldosterone-Regulated Sodium Transport and Blood Pressure.Frontiers in physiology · 2022Review
- Serum and Glucocorticoid-Inducible Kinase 1 (SGK1) in NSCLC Therapy.Pharmaceuticals (Basel, Switzerland) · 2020Review
- The Enigmatic Role of Serum & Glucocorticoid Inducible Kinase 1 in the Endometrium.Frontiers in cell and developmental biology · 2020Review
- Estrogen negatively regulates the renal epithelial sodium channel (ENaC) by promoting Derlin-1 expression and AMPK activation.Experimental & molecular medicine · 2019Article
- Review
- RNA sequencing reveals widespread transcriptome changes in a renal carcinoma cell line.Oncotarget · 2018Article
- Inhibitors of the proteasome stimulate the epithelial sodium channel (ENaC) through SGK1 and mimic the effect of aldosterone.Pflugers Archiv : European journal of physiology · 2018Article
- Glucocorticoid-induced leucine zipper protein regulates sodium and potassium balance in the distal nephron.Kidney international · 2017Article
- Potential Roles of Amiloride-Sensitive Sodium Channels in Cancer Development.BioMed research international · 2016Review
- Collecting duct principal cell transport processes and their regulation.Clinical journal of the American Society of Nephrology : CJASN · 2015Review
- GILZ as a Mediator of the Anti-Inflammatory Effects of Glucocorticoids.Frontiers in endocrinology · 2015Review
- Scaffold protein connector enhancer of kinase suppressor of Ras isoform 3 (CNK3) coordinates assembly of a multiprotein epithelial sodium channel (ENaC)-regulatory complex.The Journal of biological chemistry · 2012Article
- Epithelial Na(+) channel regulation by cytoplasmic and extracellular factors.Experimental cell research · 2012Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Serum- and glucocorticoid-induced kinase 1 (SGK1) is a multifunctional protein kinase that markedly influences various cellular processes such as proliferation, apoptosis, glucose metabolism, and sodium (Na(+)) transport via the epithelial Na(+) channel, ENaC. SGK1 is a short-lived protein, which is predominantly targeted to the endoplasmic reticulum (ER) to undergo rapid proteasome-mediated degradation through the ER-associated degradation (ERAD) system. We show here that the aldosterone-induced chaperone, GILZ1 (glucocorticoid-induced leucine zipper protein-1) selectively decreases SGK1 localization to ER as well as its interaction with ER-associated E3 ubiquitin ligases, HRD1 and CHIP. GILZ1 inhibits SGK1 ubiquitinylation and subsequent proteasome-mediated degradation, thereby prolonging its half-life and increasing its steady-state expression. Furthermore, comparison of the effect of GILZ1 with that of proteasome inhibition (by MG-132) supports the idea that these effects of GILZ1 are secondary to physical interaction of GILZ1 with SGK1 and enhanced recruitment of SGK1 to targets within an "ENaC regulatory complex," thus making less SGK1 available to the ERAD machinery. Finally, effects of GILZ1 knockdown and overexpression strongly support the idea that these effects of GILZ1 are functionally important for ENaC regulation. These data provide new insight into how the manifold activities of SGK1 are selectively deployed and strengthened through modulation of its molecular interactions, subcellular localization, and stability.
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Registered trials
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.