ArticleThe Journal of cell biology2005
STIM1, an essential and conserved component of store-operated Ca2+ channel function.
Article in The Journal of cell biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 979 papers, 1 of them a synthesis that pooled it.
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
979 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,795 citations in OpenAlex.
- Stay in touch with the endoplasmic reticulum.Science China. Life sciences · 2024Pooled it
- Mechanistic insights into Orai dynamics during pore opening.Channels (Austin, Tex.) · 2026Review
- Research progress on the role and mechanism of STIM and Orai protein-mediated store-operated calcium entry in cardiovascular diseases.Channels (Austin, Tex.) · 2026Review
- Developing Optogenetic Approaches to Study CaCold Spring Harbor perspectives in biology · 2026Review
- Evolutionarily conserved hydrophobicity and sterics in TM3/TM4 balance Orai1 pore opening.Protein science : a publication of the Protein Society · 2026Article
- Oxidative protein folding and CaCellular and molecular life sciences : CMLS · 2026Review
- A Quartet of Native Orai Channel Isoforms Orchestrates Graded NFAT Activation and Transcription.bioRxiv : the preprint server for biology · 2026Article
- Acid-sensing ion channels in the vasculature: emerging roles in systemic and pulmonary circulations.Pflugers Archiv : European journal of physiology · 2026Review
- STIM-Orai signaling in neurons: integrating calcium dynamics and synaptic plasticity.Cell communication and signaling : CCS · 2026Review
- The nonexcitable smooth muscle: remodeling the smooth muscle ion transport toolkit in disease.Physiological reviews · 2026Review
- Deletion of mitochondrial calcium uniporter enhances calcium signals by slowing calcium clearance and triggers adaptive transcriptomic remodeling.The Journal of biological chemistry · 2026Article
- Unraveling new functions of the Ca2+ sensor STIM1 in cell signaling.Biochemical Society transactions · 2026Review
- STIM1 GoF Mutants: Genotype-Phenotype Relationships Across the Stormorken/TAM/YPS Spectrum.Cells · 2026Review
- MCTP1 and MCTP2 promote ER-PM contact sites and regulate PI4P homeostasis and cell migration.Molecular biology of the cell · 2026Article
- Activation of nuclear CaCell reports · 2026Article
- Review
- A small molecule VDAC ligand inhibits ERAD and induces selective cancer cell death via disruption of calcium homeostasis.Nature communications · 2026Article
- Review
- Formation, Organization, and Maintenance of Synaptic Vesicle Pools: From Molecules to Structure and Dynamics.Advances in neurobiology · 2026Review
- Lipid Metabolism in Relation to Calcium Homeostasis.Advances in experimental medicine and biology · 2026Review
919 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Store-operated Ca2+ (SOC) channels regulate many cellular processes, but the underlying molecular components are not well defined. Using an RNA interference (RNAi)-based screen to identify genes that alter thapsigargin (TG)-dependent Ca2+ entry, we discovered a required and conserved role of Stim in SOC influx. RNAi-mediated knockdown of Stim in Drosophila S2 cells significantly reduced TG-dependent Ca2+ entry. Patch-clamp recording revealed nearly complete suppression of the Drosophila Ca2+ release-activated Ca2+ (CRAC) current that has biophysical characteristics similar to CRAC current in human T cells. Similarly, knockdown of the human homologue STIM1 significantly reduced CRAC channel activity in Jurkat T cells. RNAi-mediated knockdown of STIM1 inhibited TG- or agonist-dependent Ca2+ entry in HEK293 or SH-SY5Y cells. Conversely, overexpression of STIM1 in HEK293 cells modestly enhanced TG-induced Ca2+ entry. We propose that STIM1, a ubiquitously expressed protein that is conserved from Drosophila to mammalian cells, plays an essential role in SOC influx and may be a common component of SOC and CRAC channels.
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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.