ReviewPflugers Archiv : European journal of physiology2010
CRAC channelopathies.
Review in Pflugers Archiv : European journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
125 citing papers in PubMed, 200 citations in OpenAlex.
- Density of functional Ca2+ release-activated Ca2+ (CRAC) channels declines after T-cell activation.Channels (Austin, Tex.)Trial
- Developing Optogenetic Approaches to Study CaCold Spring Harbor perspectives in biology · 2026Review
- STIM/Orai-Mediated Store-Operated CaCells · 2026Review
- STIM1 GoF Mutants: Genotype-Phenotype Relationships Across the Stormorken/TAM/YPS Spectrum.Cells · 2026Review
- Comprehensive mutational characterization of the calcium-sensing STIM1 EF-hand reveals residues essential for structure and function.Genetics · 2025Article
- Prognostic implications of store-operated calcium entry signatures and immune dynamics in neuroblastoma via machine learning.Translational cancer research · 2025Article
- Comprehensive mutational characterization of the calcium-sensing STIM1 EF-hand reveals residues essential for structure and function.bioRxiv : the preprint server for biology · 2025Article
- Rap1A Modulates Store-Operated Calcium Entry in the Lung Endothelium: A Novel Mechanism Controlling NFAT-Mediated Vascular Inflammation and Permeability.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Regulation of T Lymphocyte Functions through Calcium Signaling Modulation by Nootkatone.International journal of molecular sciences · 2024Article
- Synthetic Biology Meets CaCells · 2024Review
- A multiple-oscillator mechanism underlies antigen-induced CaThe Journal of biological chemistry · 2023Article
- The CaBiomolecules · 2023Review
- TRPM2-mediated CaCell communication and signaling : CCS · 2023Review
- S417 in the CC3 region of STIM1 is critical for STIM1-Orai1 binding and CRAC channel activation.Life science alliance · 2023Article
- A pathogenic human Orai1 mutation unmasks STIM1-independent rapid inactivation of Orai1 channels.eLife · 2023Article
- ORAI Calcium Channels: Regulation, Function, Pharmacology, and Therapeutic Targets.Pharmaceuticals (Basel, Switzerland) · 2023Review
- The role of ion channels in T cell function and disease.Frontiers in immunology · 2023Review
- Neural stem cell self-renewal stimulation by store-operated calcium entries in adult mouse area postrema: influence of leptin.Frontiers in cellular neuroscience · 2023Article
- Article
- ORAI3 is dispensable for store-operated Ca2+ entry and immune responses by lymphocytes and macrophages.The Journal of general physiology · 2022Article
65 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
1 author at 1 institution in 1 country.
Funding
Abstract
Store-operated Ca2+ entry (SOCE) is an important Ca2+ influx pathway in many non-excitable and some excitable cells. It is regulated by the filling state of intracellular Ca2+ stores, notably the endoplasmic reticulum (ER). Reduction in [Ca2+]ER results in activation of plasma membrane Ca2+ channels that mediate sustained Ca2+ influx which is required for many cell functions as well as refilling of Ca2+ stores. The Ca2+ release activated Ca2+ (CRAC) channel is the best characterized SOC channel with well-defined electrophysiological properties. In recent years, the molecular components of the CRAC channel, long mysterious, have been defined. ORAI1 (or CRACM1) acts as the pore-forming subunit of the CRAC channel in the plasma membrane. Stromal interaction molecule (STIM) 1 is localized in the ER, senses [Ca2+]ER, and activates the CRAC channel upon store depletion by binding to ORAI1. Both proteins are widely expressed in many tissues in both human and mouse consistent with the widespread prevalence of SOCE and CRAC channel currents in many cells types. CRAC channelopathies in human patients with mutations in STIM1 and ORAI1 are characterized by abolished CRAC channel currents, lack of SOCE and-clinically-immunodeficiency, congenital myopathy, and anhydrotic ectodermal dysplasia. This article reviews the role of ORAI and STIM proteins for SOCE and CRAC channel function in a variety of cell types and tissues and compares the phenotypes of ORAI1 and STIM1-deficient human patients and mice with targeted deletion of Orai and Stim genes.
Indexed as
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What OpenQuestion holds
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.