ArticleBiochimica et biophysica acta2014
Polyunsaturated fatty acids inhibit stimulated coupling between the ER Ca(2+) sensor STIM1 and the Ca(2+) channel protein Orai1 in a process that correlates with inhibition of stimulated STIM1 oligomerization.
Article in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Altered plasma fatty acids composition in autism spectrum disorder: a case-control study.Frontiers in psychiatry · 2025Article
- Role of STIM1 in the Regulation of Cardiac Energy Substrate Preference.International journal of molecular sciences · 2023Review
- Understanding doxorubicin associated calcium remodeling during triple-negative breast cancer treatment: anExploration of targeted anti-tumor therapy · 2021Article
- Molecular Choreography and Structure of CaMembranes · 2020Review
- Novel role of the ER/SR CaAmerican journal of physiology. Heart and circulatory physiology · 2019Article
- Molecular anatomy of the early events in STIM1 activation - oligomerization or conformational change?Journal of cell science · 2017Article
- Roles for lipid heterogeneity in immunoreceptor signaling.Biochimica et biophysica acta · 2016Review
- Store-operated CRAC channel inhibitors: opportunities and challenges.Future medicinal chemistry · 2016Review
- Roles for Ca2+ mobilization and its regulation in mast cell functions: recent progress.Biochemical Society transactions · 2016Review
- Defective lipid metabolism in neurodegeneration with brain iron accumulation (NBIA) syndromes: not only a matter of iron.Journal of inherited metabolic disease · 2015Review
- STIM1 activation is regulated by a 14 amino acid sequence adjacent to the CRAC activation domain.AIMS biophysicsArticle
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Polyunsaturated fatty acids (PUFAs) have been found to be effective inhibitors of cell signaling in numerous contexts, and we find that acute addition of micromolar PUFAs such as linoleic acid effectively inhibit of Ca(2+) responses in mast cells stimulated by antigen-mediated crosslinking of FcεRI or by the SERCA pump inhibitor, thapsigargin. In contrast, the saturated fatty acid, stearic acid, with the same carbon chain length as linoleic acid does not inhibit these responses. Consistent with this inhibition of store-operated Ca(2+) entry (SOCE), linoleic acid inhibits antigen-stimulated granule exocytosis to a similar extent. Using the fluorescently labeled plasma membrane Ca(2+) channel protein, AcGFP-Orai1, together with the labeled ER Ca(2+) sensor protein, STIM1-mRFP, we monitor stimulated coupling of these proteins that is essential for SOCE with a novel spectrofluorimetric resonance energy transfer method. We find effective inhibition of this stimulated coupling by linoleic acid that accounts for the inhibition of SOCE. Moreover, we find that linoleic acid induces some STIM1-STIM1 association, while inhibiting stimulated STIM1 oligomerization that precedes STIM1-Orai1 coupling. We hypothesize that linoleic acid and related PUFAs inhibit STIM1-Orai1 coupling by a mechanism that involves perturbation of ER membrane structure, possibly by disrupting electrostatic interactions important in STIM1 oligomerization. Thisarticle is part of a Special Issue entitled Tools to study lipid functions.
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