ArticleJournal of the American Society of Nephrology : JASN2014
Claudin-14 underlies Ca⁺⁺-sensing receptor-mediated Ca⁺⁺ metabolism via NFAT-microRNA-based mechanisms.
Article in Journal of the American Society of Nephrology : JASN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 92 citations in OpenAlex.
- Association of serum magnesium and calcium with metabolic syndrome: a cross-sectional study from the Qatar-biobank.Nutrition & metabolism · 2025Article
- Calcium signalling and transport in the kidney.Nature reviews. Nephrology · 2024Review
- Non-Coding RNAs in Kidney Stones.Biomolecules · 2024Review
- The role of claudins in homeostasis.Nature reviews. Nephrology · 2023Review
- Physiology of a Forgotten Electrolyte-Magnesium Disorders.Advances in kidney disease and health · 2023Review
- Epidemiology, Pathophysiology, and Genetics of Primary Hyperparathyroidism.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022Review
- The importance of kidney calcium handling in the homeostasis of extracellular fluid calcium.Pflugers Archiv : European journal of physiology · 2022Review
- Claudins in kidney health and disease.Kidney research and clinical practice · 2022Article
- Molecular mechanisms altering tubular calcium reabsorption.Pediatric nephrology (Berlin, Germany) · 2022Review
- Pathophysiological aspects of the thick ascending limb and novel genetic defects: HELIX syndrome and transient antenatal Bartter syndrome.Pediatric nephrology (Berlin, Germany) · 2022Review
- Extracellular Calcium Receptor as a Target for Glutathione and Its Derivatives.International journal of molecular sciences · 2022Review
- Association study ofOpen life sciences · 2022Article
- Activation of the calcium sensing receptor increases claudin-14 expression via a PLC -p38-Sp1 pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Photoperiod-dependent developmental reprogramming of the transcriptional response to seawater entry in Atlantic salmon (Salmo salar).G3 (Bethesda, Md.) · 2021Article
- Tight junctions and their regulation by non-coding RNAs.International journal of biological sciences · 2021Review
- Genetic polymorphisms in CLDN14 (rs219780) and ALP (rs1256328) genes are associated with risk of nephrolithiasis in Egyptian children.Turkish journal of urology · 2021Article
- Review
- International Union of Basic and Clinical Pharmacology. CVIII. Calcium-Sensing Receptor Nomenclature, Pharmacology, and Function.Pharmacological reviews · 2020Review
- Claudins in Renal Physiology and Pathology.Genes · 2020Review
- Mouse Models of Human Claudin-Associated Disorders: Benefits and Limitations.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 3 countries.
Funding
Abstract
Pathologic dysregulation of extracellular calcium metabolism is difficult to correct. The extracellular Ca(++)-sensing receptor (CaSR), a G protein-coupled receptor that regulates renal Ca(++) handling through changes in paracellular channel permeability in the thick ascending limb, has emerged as an effective pharmacological candidate for managing calcium metabolism. However, manipulation of CaSR at the systemic level causes promiscuous effects in the parathyroid glands, kidneys, and other tissues, and the mechanisms by which CaSR regulates paracellular transport in the kidney remain unknown. Here, we describe a CaSR-NFATc1-microRNA-claudin-14 signaling pathway in the kidney that underlies paracellular Ca(++) reabsorption through the tight junction. With CaSR-specific pharmacological reagents, we show that the in vivo gene expression of claudin-14 is regulated through a transcriptional mechanism mediated by NFATc1-microRNA and associated chromatin remodeling. Transgenic knockout and overexpression approaches showed that claudin-14 is required for CaSR-regulated renal Ca(++) metabolism. Together, our results define an important signaling cascade that, when dysregulated, may mediate Ca(++) imbalance through changes in tight junction permeability.
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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.