ReviewPhysiological reviews2015
Store-Operated Calcium Channels.
Review in Physiological reviews, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 741 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
741 citing papers in PubMed.
- Store-operated calcium signaling modulators improve a dendritic cell-based vaccine against melanoma.Oncoimmunology · 2026Article
- Ion-GPS nanocapsules activate calcium-permeable gates in inflammatory microglia for nerve function recovery.Bioactive materials · 2026Article
- Mechanistic insights into Orai dynamics during pore opening.Channels (Austin, Tex.) · 2026Review
- Organelle contact reorganization drives calcium-dependent autophagy under proteostatic stress.Autophagy · 2026Article
- Calcium signaling in microglial immune functions: current understanding and implications for disease.Current opinion in immunology · 2026Review
- Glial cells in neuropathic pain.Physiological reviews · 2026Review
- Prohibitin controls MRS2-Mediated mitochondrial MgCell reports · 2026Article
- A supramolecular complex of palmitoylated Orai C-terminal peptide and cyclodextrin targets the plasma membrane to reduce store-operated calcium channel activity.Materials advances · 2026Article
- Hypercapnia enhances airway smooth muscle contractility via STIM1-dependent Ca2+ signaling.JCI insight · 2026Article
- The interaction between NPMc+ and Orai1 induces abnormal calcium influx to facilitate leukemogenesis.The FEBS journal · 2026Article
- Pyrazole-derived TRPC3 antagonist ameliorates synaptic dysfunctions and memory deficits in Alzheimer's disease models.Molecular psychiatry · 2026Article
- Ginsenoside Compound K Differentially Regulates Neuronal and Astrocytic CaPharmaceuticals (Basel, Switzerland) · 2026Article
- Calcium dysregulation in neurovascular function in Alzheimer's disease: mechanisms, therapeutic targets.GeroScience · 2026Review
- Developing Optogenetic Approaches to Study CaCold Spring Harbor perspectives in biology · 2026Review
- Specialized cortical ER architecture modulates CaiScience · 2026Article
- Orai1-mediated CaExperimental & molecular medicine · 2026Article
- Evolutionarily conserved hydrophobicity and sterics in TM3/TM4 balance Orai1 pore opening.Protein science : a publication of the Protein Society · 2026Article
- Ryanodine Receptor 1 Is Dispensable for CD4European journal of immunology · 2026Article
- Dysregulated calcium signaling underlies hyposalivation and microbial dysbiosis in Down syndrome.Cell reports · 2026Article
- iPLAScience advances · 2026Article
681 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Store-operated calcium channels (SOCs) are a major pathway for calcium signaling in virtually all metozoan cells and serve a wide variety of functions ranging from gene expression, motility, and secretion to tissue and organ development and the immune response. SOCs are activated by the depletion of Ca(2+) from the endoplasmic reticulum (ER), triggered physiologically through stimulation of a diverse set of surface receptors. Over 15 years after the first characterization of SOCs through electrophysiology, the identification of the STIM proteins as ER Ca(2+) sensors and the Orai proteins as store-operated channels has enabled rapid progress in understanding the unique mechanism of store-operate calcium entry (SOCE). Depletion of Ca(2+) from the ER causes STIM to accumulate at ER-plasma membrane (PM) junctions where it traps and activates Orai channels diffusing in the closely apposed PM. Mutagenesis studies combined with recent structural insights about STIM and Orai proteins are now beginning to reveal the molecular underpinnings of these choreographic events. This review describes the major experimental advances underlying our current understanding of how ER Ca(2+) depletion is coupled to the activation of SOCs. Particular emphasis is placed on the molecular mechanisms of STIM and Orai activation, Orai channel properties, modulation of STIM and Orai function, pharmacological inhibitors of SOCE, and the functions of STIM and Orai in physiology and disease.
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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.