ArticleThe Journal of physiology2005
Capacitative calcium entry supports calcium oscillations in human embryonic kidney cells.
Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.
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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.
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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
71 citing papers in PubMed, 1 synthesis or guideline pooled it, 129 citations in OpenAlex.
- A Reappraisal of the Effects of L-type CaFunction (Oxford, England) · 2023Pooled it
- Latrophilin-1-Mediated GCells · 2026Article
- Calcium Signaling in Cardiac Fibroblasts: Roles in Fibrosis and Therapeutic Implications.Cardiovascular drugs and therapy · 2026Review
- L-type calcium channel blockers at therapeutic concentrations are not linked to CRAC channels and heart failure.Clinical and experimental hypertension (New York, N.Y. : 1993) · 2025Article
- Two-pore domain potassium channel TREK-1 contributes to arachidonic acid-induced CaBiochemistry and biophysics reports · 2025Article
- A molecular systems perspective on calcium oscillations beyond ion fluxes.Current opinion in cell biology · 2025Review
- An integrate-and-fire approach to CaBiophysical journal · 2023Article
- ORAI Calcium Channels: Regulation, Function, Pharmacology, and Therapeutic Targets.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Plasma Membrane CaFunction (Oxford, England) · 2022Article
- Multifunctional Liposomes Modulate Purinergic Receptor-Induced Calcium Wave in Cerebral Microvascular Endothelial Cells and Astrocytes: New Insights for Alzheimer's disease.Molecular neurobiology · 2021Article
- Omnitemporal choreographies of all five STIM/Orai and IPCell reports · 2021Article
- Signaling through CaCold Spring Harbor perspectives in biology · 2020Review
- Endoplasmic Reticulum Calcium Pumps and Tumor Cell Differentiation.International journal of molecular sciences · 2020Review
- The Endoplasmic Reticulum-Plasma Membrane Junction: A Hub for Agonist Regulation of CaCold Spring Harbor perspectives in biology · 2020Review
- Changes in Calcium Homeostasis and Gene Expression Implicated in Epilepsy in Hippocampi of Mice OverexpressingInternational journal of molecular sciences · 2019Article
- Store-operated CaBiochimica et biophysica acta. Molecular cell research · 2019Article
- Constitutive IPJournal of cell science · 2019Article
- Calcium influx and sperm-evoked calcium responses during oocyte maturation and egg activation.Oncotarget · 2017Review
- Ratiometric Matryoshka biosensors from a nested cassette of green- and orange-emitting fluorescent proteins.Nature communications · 2017Article
- Store-operated CaCell calcium · 2017Article
11 more citing papers are in PubMed but not listed here.
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2 authors at 1 institution in 1 country.
Funding
Abstract
Treatment of human epithelial kidney (HEK293) cells with low concentrations of the muscarinic agonist methacholine results in the activation of complex and repetitive cycling of intracellular calcium ([Ca(2+)](i)), known as [Ca(2+)](i) oscillations. These oscillations occur with a frequency that depends on the concentration of methacholine, whereas the magnitude of the [Ca(2+)](i) spikes does not. The oscillations do not persist in the absence of extracellular Ca(2+), leading to the conclusion that entry of Ca(2+) across the plasma membrane plays a significant role in either their initiation or maintenance. However, treatment of cells with high concentrations of GdCl(3), a condition which limits the flux of calcium ions across the plasma membrane in both directions, allows sustained [Ca(2+)](i) oscillations to occur. This suggests that the mechanisms that both initiate and regenerate [Ca(2+)](i) oscillations are intrinsic to the intracellular milieu and do not require entry of extracellular Ca(2+). This would additionally suggest that, under normal conditions, the role of calcium entry is to sustain [Ca(2+)](i) oscillations. By utilizing relatively specific pharmacological manoeuvres we provide evidence that the Ca(2+) entry that supports Ca(2+) oscillations occurs through the store-operated or capacitative calcium entry pathway. However, by artificial introduction of a non-store-operated pathway into the cells (TRPC3 channels), we find that other Ca(2+) entry mechanisms can influence oscillation frequency in addition to the store-operated channels.
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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.