ArticleThe EMBO journal2008
Invalidation of TASK1 potassium channels disrupts adrenal gland zonation and mineralocorticoid homeostasis.
Article in The EMBO journal, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.
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Who cites it
77 citing papers in PubMed, 1 synthesis or guideline pooled it, 192 citations in OpenAlex.
- Identification of risk loci for primary aldosteronism in genome-wide association studies.Nature communications · 2022Pooled it
- Rare germline variants in canonical and candidate genes in apparently sporadic bilateral primary aldosteronism.Journal of the Endocrine Society · 2026Article
- K2P channels as emerging therapeutic targets for pain: insights from functional studies and transcriptomic analyses.Frontiers in pharmacology · 2026Review
- Osmolarity Controls Oscillatory Calcium Signaling to Reduce Autonomous Aldosterone Production in Zona Glomerulosa Cells.Endocrinology · 2025Article
- Article
- LDLRAD4 is a potential diagnostic and prognostic biomarker correlated with immune infiltration in myelodysplastic syndromes.Frontiers in genetics · 2025Article
- Transcriptome analyses reveal common immune system dysregulation in PAH patients andPulmonary circulation · 2024Article
- Chronic activation of adrenal Gq signaling induces Cyp11b2 expression in the zona fasciculata and hyperaldosteronism.Molecular and cellular endocrinology · 2024Article
- T- and L-Type Calcium Channels Maintain Calcium Oscillations in the Murine Zona Glomerulosa.Hypertension (Dallas, Tex. : 1979) · 2024Article
- Expression and function of mitochondrial inhibitor factor-1 and TASK channels in adrenal cells.Biochemical and biophysical research communications · 2023Article
- Intrinsic Adrenal TWIK-Related Acid-Sensitive TASK Channel Dysfunction Produces Spontaneous Calcium Oscillations Sufficient to Drive AngII (Angiotensin II)-Unresponsive Hyperaldosteronism.Hypertension (Dallas, Tex. : 1979) · 2022Article
- Potassium homeostasis: sensors, mediators, and targets.Pflugers Archiv : European journal of physiology · 2022Review
- Aldosterone-Regulated Sodium Transport and Blood Pressure.Frontiers in physiology · 2022Review
- Ectopic localization of CYP11B1 and CYP11B2-expressing cells in the normal human adrenal gland.PloS one · 2022Article
- Molecular Mechanisms of Functional Adrenocortical Adenoma and Carcinoma: Genetic Characterization and Intracellular Signaling Pathway.Biomedicines · 2021Review
- The Sexually Dimorphic Adrenal Cortex: Implications for Adrenal Disease.International journal of molecular sciences · 2021Review
- Ion Channel Function and Electrical Excitability in the Zona Glomerulosa: A Network Perspective on Aldosterone Regulation.Annual review of physiology · 2021Review
- The Experimental TASK-1 Potassium Channel Inhibitor A293 Can Be Employed for Rhythm Control of Persistent Atrial Fibrillation in a Translational Large Animal Model.Frontiers in physiology · 2021Article
- TASK channels: channelopathies, trafficking, and receptor-mediated inhibition.Pflugers Archiv : European journal of physiology · 2020Review
- TASK-1 and TASK-3 channels modulate pressure overload-induced cardiac remodeling and dysfunction.American journal of physiology. Heart and circulatory physiology · 2020Article
17 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
20 authors at 8 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TASK1 (KCNK3) and TASK3 (KCNK9) are two-pore domain potassium channels highly expressed in adrenal glands. TASK1/TASK3 heterodimers are believed to contribute to the background conductance whose inhibition by angiotensin II stimulates aldosterone secretion. We used task1-/- mice to analyze the role of this channel in adrenal gland function. Task1-/- exhibited severe hyperaldosteronism independent of salt intake, hypokalemia, and arterial 'low-renin' hypertension. The hyperaldosteronism was fully remediable by glucocorticoids. The aldosterone phenotype was caused by an adrenocortical zonation defect. Aldosterone synthase was absent in the outer cortex normally corresponding to the zona glomerulosa, but abundant in the reticulo-fasciculata zone. The impaired mineralocorticoid homeostasis and zonation were independent of the sex in young mice, but were restricted to females in adults. Patch-clamp experiments on adrenal cells suggest that task3 and other K+ channels compensate for the task1 absence. Adrenal zonation appears as a dynamic process that even can take place in adulthood. The striking changes in the adrenocortical architecture in task1-/- mice are the first demonstration of the causative role of a potassium channel in development/differentiation.
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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.