ArticleBioscience reports2013
Oligomerization and Ca2+/calmodulin control binding of the ER Ca2+-sensors STIM1 and STIM2 to plasma membrane lipids.
Article in Bioscience reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 54 citations in OpenAlex.
- Research progress on the role and mechanism of STIM and Orai protein-mediated store-operated calcium entry in cardiovascular diseases.Channels (Austin, Tex.) · 2026Review
- STIM-Orai signaling in neurons: integrating calcium dynamics and synaptic plasticity.Cell communication and signaling : CCS · 2026Review
- STIM1-containing contact sites promote direct calcium flux from the endoplasmic reticulum to mitochondria.The EMBO journal · 2026Article
- Structural rearrangements underlying the activation of STIM1 by ER calcium depletion.bioRxiv : the preprint server for biology · 2026Article
- Article
- STIM Proteins and Regulation of SOCE in ER-PM Junctions.Biomolecules · 2022Review
- Control of STIM and Orai function by post-translational modifications.Cell calcium · 2022Review
- Extraction and Prioritization of a Gene-Cancer-By-Survival Network Involved in Homeostasis of Intracellular Calcium Concentrations Using TCGA PANCAN Data.Bioelectricity · 2022Article
- The Role of Lipids in CRAC Channel Function.Biomolecules · 2022Review
- STIM and Orai Mediated Regulation of Calcium Signaling in Age-Related Diseases.Frontiers in aging · 2022Review
- Review
- Regulation of Store-Operated CaCells · 2021Review
- Endoplasmic Reticulum-Plasma Membrane Contact Sites as an Organizing Principle for Compartmentalized Calcium and cAMP Signaling.International journal of molecular sciences · 2021Review
- Proteins Interacting with STIM1 and Store-Operated CaProgress in molecular and subcellular biology · 2021Review
- STIM2 targets Orai1/STIM1 to the AKAP79 signaling complex and confers coupling of CaProceedings of the National Academy of Sciences of the United States of America · 2020Article
- The Endoplasmic Reticulum-Plasma Membrane Junction: A Hub for Agonist Regulation of CaCold Spring Harbor perspectives in biology · 2020Review
- Lipid-dependent coupling of secretory cargo sorting and trafficking at the trans-Golgi network.FEBS letters · 2019Review
- Numbers count: How STIM and Orai stoichiometry affect store-operated calcium entry.Cell calcium · 2019Review
- Cross-talk between N-terminal and C-terminal domains in stromal interaction molecule 2 (STIM2) determines enhanced STIM2 sensitivity.The Journal of biological chemistry · 2019Article
- Protein Amphipathic Helix Insertion: A Mechanism to Induce Membrane Fission.Frontiers in cell and developmental biology · 2019Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ca2+ (calcium) homoeostasis and signalling rely on physical contacts between Ca2+ sensors in the ER (endoplasmic reticulum) and Ca2+ channels in the PM (plasma membrane). STIM1 (stromal interaction molecule 1) and STIM2 Ca2+ sensors oligomerize upon Ca2+ depletion in the ER lumen, contact phosphoinositides at the PM via their cytosolic lysine (K)-rich domains, and activate Ca2+ channels. Differential sensitivities of STIM1 and STIM2 towards ER luminal Ca2+ have been studied but responses towards elevated cytosolic Ca2+ concentration and the mechanism of lipid binding remain unclear. We found that tetramerization of the STIM1 K-rich domain is necessary for efficient binding to PI(4,5)P2-containing PM-like liposomes consistent with an oligomerization-driven STIM1 activation. In contrast, dimerization of STIM2 K-rich domain was sufficient for lipid binding. Furthermore, the K-rich domain of STIM2, but not of STIM1, forms an amphipathic α-helix. These distinct features of the STIM2 K-rich domain cause an increased affinity for PI(4,5)P2, consistent with the lower activation threshold of STIM2 and a function as regulator of basal Ca2+ levels. Concomitant with higher affinity for PM lipids, binding of CaM (calmodulin) inhibited the interaction of the STIM2 K-rich domain with liposomes in a Ca2+ and PI(4,5)P2 concentration-dependent manner. Therefore we suggest that elevated cytosolic Ca2+ concentration down-regulates STIM2-mediated ER-PM contacts via CaM binding.
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