ArticleScientific reports2015
Retrograde regulation of STIM1-Orai1 interaction and store-operated Ca2+ entry by calsequestrin.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 54 citations in OpenAlex.
- Review
- The emerging role of calsequestrin 2: from calcium sensor and modulator to arrhythmia driver.Journal of physiology and biochemistry · 2026Review
- Review
- Characterization of novel CASQ1 variants in two families with unusual phenotypic features.Journal of neurology · 2025Article
- Estrogens and Antioxidants Prevent the Formation of Tubular Aggregates in Aging Male Mice.International journal of molecular sciences · 2025Article
- ERG1A KScientific reports · 2025Article
- TAM-associated CASQ1 mutants diminish intracellular CaJournal of muscle research and cell motility · 2024Article
- Sarcoplasmic Reticulum CaCells · 2023Review
- CASQ1-related myopathy: The first report from China and the literature review.Clinical case reports · 2022Article
- Mutations in proteins involved in E-C coupling and SOCE and congenital myopathies.The Journal of general physiology · 2022Review
- Ryanodine receptor 1 (RYR1) mutations in two patients with tubular aggregate myopathy.The European journal of neuroscience · 2022Article
- Ablation of Calsequestrin-1, CaFrontiers in physiology · 2022Review
- Article
- Sigma-1 Receptor Ligands Chlorpromazine and Trifluoperazine Attenuate CaCell and tissue biology · 2022Article
- Calsequestrin 1 Is an Active Partner of Stromal Interaction Molecule 2 in Skeletal Muscle.Cells · 2021Article
- Review
- Article
- Improper Remodeling of Organelles Deputed to CaInternational journal of molecular sciences · 2021Review
- Calsequestrin, a key protein in striated muscle health and disease.Journal of muscle research and cell motility · 2021Review
- Calcium entry units (CEUs): perspectives in skeletal muscle function and disease.Journal of muscle research and cell motility · 2021Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Interaction between the endoplasmic reticulum (ER)-located stromal interaction molecue1 (STIM1) and the plasma membrane-located Ca(2+) channel subunit, Orai1, underlies store-operated Ca(2+) entry (SOCE). Calsequestrin1 (CSQ1), a sarcoplasmic reticulum Ca(2+) buffering protein, inhibits SOCE, but the mechanism of action is unknown. We identified an interaction between CSQ1 and STIM1 in HEK293 cells. An increase in monomeric CSQ1 induced by depleted Ca(2+) stores, or trifluoperazine (TFP), a blocker of CSQ folding and aggregation, enhanced the CSQ1-STIM1 interaction. In cells with Ca(2+) stores depleted, TFP further increased CSQ1 monomerization and CSQ1-STIM1 interaction, but reduced the association of STIM1 with Orai1 and SOCE. Over-expression of CSQ1 or a C-terminal (amino acid 388-396) deletion mutant significantly promoted the association of CSQ1 with STIM1, but suppressed both STIM1-Orai1 interaction and SOCE, while over-expression of the C-terminal (amino acid 362-396) deletion mutant had no effect. The physical interaction between low polymeric forms of CSQ1 and STIM1 likely acts by interfering with STIM1 oligimerization and inhibits STIM1-Orai1 interaction, providing a brake to SOCE under physiological conditions. This novel regulatory mechanism for SOCE may also contribute to the pathological Ca(2+) overload in calsequestrin deficient diseases, such as malignant hyperthermia and ventricular tachycardia.
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