ArticleProceedings of the National Academy of Sciences of the United States of America2001
A zinc-sensing receptor triggers the release of intracellular Ca2+ and regulates ion transport.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 1 of them a synthesis that pooled it.
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Who cites it
89 citing papers in PubMed, 1 synthesis or guideline pooled it, 255 citations in OpenAlex.
- The effects of vitamin and mineral supplementation on women with gestational diabetes mellitus.BMC endocrine disorders · 2021Pooled it
- Novel Roles of GPCRs in the Renal Collecting Duct.Physiology (Bethesda, Md.) · 2026Review
- In Vitro Evaluation of Anti-Inflammatory and Antioxidant Properties of a Novel Calcium Alginate-Zinc Hemostatic Biomaterial.Journal of functional biomaterials · 2026Article
- Selective Pharmacological Blockade of GPR39 Markedly Reduces No Reflow and Infarct Volumes in a Rat Model of Acute Myocardial Infarction.bioRxiv : the preprint server for biology · 2026Article
- Zinc, type 2 diabetes, diabetic kidney disease: focus on hypoxia.Frontiers in endocrinology · 2026Review
- Review
- Zinc inhibits cAMP-induced ClAmerican journal of physiology. Cell physiology · 2025Article
- Amorphous calcium zinc phosphate promotes macrophage-driven alveolar bone regeneration via modulation of energy metabolism and mitochondrial homeostasis.Bioactive materials · 2025Article
- Zrt-Irt-like Proteins (ZIP) Family Zinc Transporters: Emerging Players in Pancreatic β Cell Function and Insulin Regulation.The Journal of nutrition · 2025Review
- Increase of Intracellular Zinc Levels Rather Than Zinc Influx Inhibits Interleukin-2 Production in Zinc Supplemented Jurkat Cells.Cell biochemistry and function · 2025Article
- Bitter Taste Receptor TAS2R43 Co-Regulates Mechanisms of Gastric Acid Secretion and Zinc Homeostasis.International journal of molecular sciences · 2025Article
- Targeting GPR39 in structure-based drug discovery reduces Ang II-induced hypertension.Communications biology · 2024Article
- Current advances in photocatalytic proximity labeling.Cell chemical biology · 2024Review
- Unlocking the Potential of Obestatin: A Novel Peptide Intervention for Skeletal Muscle Regeneration and Prevention of Atrophy.Molecular biotechnology · 2024Review
- Ca2+ fortified oral rehydration solution is effective in reducing diarrhea morbidity in cholera toxin-pretreated mice.Research square · 2023Article
- What Are the Functions of Zinc in the Nervous System?Neurology · 2023Article
- Zinc Acts Synergistically with Berberine for Enhancing Its Efficacy as an Anti-cancer Agent by Inducing Clusterin-Dependent Apoptosis in HT-29 Colorectal Cancer Cells.Biological trace element research · 2023Article
- Reply to Doboszewska et al.: The many faces of G-protein-coupled receptor 39.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- GPR39 deorphanization: The long and winding road to eicosanoids and a crosstalk between GPR39 and hedgehog signaling in angiogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- The role of Zn2+ in shaping intracellular Ca2+ dynamics in the heart.The Journal of general physiology · 2023Review
29 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Changes in extracellular zinc concentration participate in modulating fundamental cellular processes such as proliferation, secretion, and ion transport in a mechanism that is not well understood. Here, we show that a micromolar concentration of extracellular zinc triggers a massive release of calcium from thapsigargin-sensitive intracellular pools in the colonocytic cell line HT29. Calcium release was blocked by a phospholipase-C inhibitor, indicating that formation of inositol 1,4,5-triphosphate is required for zinc-dependent calcium release. Zinc influx was not observed, indicating that extracellular zinc triggered the release. The Ca(i)2+ release was zinc specific and could not be triggered by other heavy metals. Furthermore, zinc failed to activate the Ca(2+)-sensing receptor heterologously expressed in HEK293 cells. The zinc-induced Ca(i)2+ rise stimulated the activity of the Na(+)/H(+) exchanger in HT29 cells. Our results indicate that a previously uncharacterized extracellular, G protein-coupled, Zn(2+)-sensing receptor is functional in colonocytes. Because Ca(i)2+ rise is known to regulate key cellular and signal-transduction processes, the zinc-sensing receptor may provide the missing link between extracellular zinc concentration changes and the regulation of cellular processes.
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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.