ArticleNature communications2016
Store-independent modulation of Ca(2+) entry through Orai by Septin 7.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 33 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
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- The role of septin 7 in physiology and pathological disease: A systematic review of current status.Journal of cellular and molecular medicine · 2018Pooled it
- Article
- Septins as key players in spermatogenesis, fertilisation and pre-implantation embryogenic cytoplasmic dynamics.Cell communication and signaling : CCS · 2024Review
- Pharmacological modulation of septins restores calcium homeostasis and is neuroprotective in models of Alzheimer's disease.Science (New York, N.Y.) · 2024Article
- Neuronal Store-Operated Calcium Channels.Molecular neurobiology · 2023Review
- Regulation of store-operated CaeLife · 2023Article
- Article
- CRAC and SK Channels: Their Molecular Mechanisms Associated with Cancer Cell Development.Cancers · 2022Review
- Article
- Article
- Septins tune lipid kinase activity and PI(4,5)PLife science alliance · 2022Article
- The Role of Lipids in CRAC Channel Function.Biomolecules · 2022Review
- Glial ER and GAP junction mediated CaGlia · 2022Article
- Editorial: Emerging Functions of Septins-Volume II.Frontiers in cell and developmental biology · 2022Article
- Septins, a cytoskeletal protein family, with emerging role in striated muscle.Journal of muscle research and cell motility · 2021Review
- Endoplasmic Reticulum-Plasma Membrane Contact Sites as an Organizing Principle for Compartmentalized Calcium and cAMP Signaling.International journal of molecular sciences · 2021Review
- Purkinje Neurons with Loss of STIM1 Exhibit Age-Dependent Changes in Gene Expression and Synaptic Components.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- More Than Just Simple Interaction between STIM and Orai Proteins: CRAC Channel Function Enabled by a Network of Interactions with Regulatory Proteins.International journal of molecular sciences · 2021Review
- Deficits Associated With Loss of STIM1 in Purkinje Neurons Including Motor Coordination Can Be Rescued by Loss of Septin 7.Frontiers in cell and developmental biology · 2021Article
- Molecular Choreography and Structure of CaMembranes · 2020Review
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Orai channels are required for store-operated Ca(2+) entry (SOCE) in multiple cell types. Septins are a class of GTP-binding proteins that function as diffusion barriers in cells. Here we show that Septin 7 acts as a 'molecular brake' on activation of Orai channels in Drosophila neurons. Lowering Septin 7 levels results in dOrai-mediated Ca(2+) entry and higher cytosolic Ca(2+) in resting neurons. This Ca(2+) entry is independent of depletion of endoplasmic reticulum Ca(2+) stores and Ca(2+) release through the inositol-1,4,5-trisphosphate receptor. Importantly, store-independent Ca(2+) entry through Orai compensates for reduced SOCE in the Drosophila flight circuit. Moreover, overexpression of Septin 7 reduces both SOCE and flight duration, supporting its role as a negative regulator of Orai channel function in vivo. Septin 7 levels in neurons can, therefore, alter neural circuit function by modulating Orai function and Ca(2+) homeostasis.
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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.