ArticleFrontiers in cell and developmental biology2021
STIM2 Mediates Excessive Store-Operated Calcium Entry in Patient-Specific iPSC-Derived Neurons Modeling a Juvenile Form of Huntington's Disease.
Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- STIM-Orai signaling in neurons: integrating calcium dynamics and synaptic plasticity.Cell communication and signaling : CCS · 2026Review
- Dysregulation of store-operated calcium entry in fibroblast lines from adult and juvenile-onset Huntington's disease patients.Pharmacological reports : PR · 2026Article
- Article
- 1,2,3,4-Dithiadiazole Derivative 3-(4-Nitrophenyl)-5-Phenyl-3H-1,2,3,4-Dithiadiazole-2-Oxide Affects Both STIM1- and STIM2-Dependent Store-Operated Calcium Channels.Bulletin of experimental biology and medicine · 2025Article
- STIM Proteins: The Gas and Brake of Calcium Entry in Neurons.Neuroscience bulletin · 2025Review
- Transcriptomic profiling of neural cultures from the KYOU iPSC line via alternative differentiation protocols.Frontiers in molecular neuroscience · 2025Article
- Calcium Ions in the Physiology and Pathology of the Central Nervous System.International journal of molecular sciences · 2024Review
- Calcium channel signalling at neuronal endoplasmic reticulum-plasma membrane junctions.Biochemical Society transactions · 2024Review
- STIM2 is involved in the regulation of apoptosis and the cell cycle in normal and malignant monocytic cells.Molecular oncology · 2024Article
- SOCE as a regulator of neuronal activity.The Journal of physiology · 2024Review
- Article
- An Efficient 2D Protocol for Differentiation of iPSCs into Mature Postmitotic Dopaminergic Neurons: Application for Modeling Parkinson's Disease.International journal of molecular sciences · 2023Article
- iPSC-derived cells lack immune tolerance to autologous NK-cells due to imbalance in ligands for activating and inhibitory NK-cell receptors.Stem cell research & therapy · 2023Article
- The Role of Voltage-Gated Calcium Channels in Basal Ganglia Neurodegenerative Disorders.Current neuropharmacology · 2023Review
- The Mystery of EVP4593: Perspectives of the Quinazoline-Derived Compound in the Treatment of Huntington's Disease and Other Human Pathologies.International journal of molecular sciences · 2022Review
- The STIM1/2-Regulated Calcium Homeostasis Is Impaired in Hippocampal Neurons of the 5xFAD Mouse Model of Alzheimer's Disease.International journal of molecular sciences · 2022Article
- Differential expression and roles of Huntingtin and Huntingtin-associated protein 1 in the mouse and primate brains.Cellular and molecular life sciences : CMLS · 2022Article
- Patient-Specific iPSCs-Based Models of Neurodegenerative Diseases: Focus on Aberrant Calcium Signaling.International journal of molecular sciences · 2022Review
- Huntington's disease iPSC models-using human patient cells to understand the pathology caused by expanded CAG repeats.Faculty reviews · 2022Review
- STIM and Orai Mediated Regulation of Calcium Signaling in Age-Related Diseases.Frontiers in aging · 2022Review
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's disease (HD) is a severe autosomal-dominant neurodegenerative disorder caused by a mutation within a gene, encoding huntingtin protein. Here we have used the induced pluripotent stem cell technology to produce patient-specific terminally differentiated GABA-ergic medium spiny neurons modeling a juvenile form of HD (HD76). We have shown that calcium signaling is dramatically disturbed in HD76 neurons, specifically demonstrating higher levels of store-operated and voltage-gated calcium uptakes. However, comparing the HD76 neurons with the previously described low-repeat HD models, we have demonstrated that the severity of calcium signaling alterations does not depend on the length of the polyglutamine tract of the mutant huntingtin. Here we have also observed greater expression of huntingtin and an activator of store-operated calcium channels STIM2 in HD76 neurons. Since shRNA-mediated suppression of STIM2 decreased store-operated calcium uptake, we have speculated that high expression of STIM2 underlies the excessive entry through store-operated calcium channels in HD pathology. Moreover, a previously described potential anti-HD drug EVP4593 has been found to attenuate high levels of both huntingtin and STIM2 that may contribute to its neuroprotective effect. Our results are fully supportive in favor of the crucial role of calcium signaling deregulation in the HD pathogenesis and indicate that the cornerstone of excessive calcium uptake in HD-specific neurons is a calcium sensor and store-operated calcium channels activator STIM2, which should become a molecular target for medical treatment and novel neuroprotective drug development.
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