ArticleFrontiers in molecular neuroscience2013
Expression of genes encoding the calcium signalosome in cellular and transgenic models of Huntington's disease.
Article in Frontiers in molecular neuroscience, 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, 48 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
- Calcium Ions in the Physiology and Pathology of the Central Nervous System.International journal of molecular sciences · 2024Review
- Genome-wide transcriptome profiling and development of age prediction models in the human brain.Aging · 2024Article
- Pathogenetic Contributions and Therapeutic Implications of Transglutaminase 2 in Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- Targeting of Calbindin 1 rescues erythropoiesis in a human model of Diamond Blackfan anemia.Blood cells, molecules & diseases · 2023Article
- Small-Molecule Disruptors of Mutant Huntingtin-Calmodulin Protein-Protein Interaction Attenuate Deleterious Effects of Mutant Huntingtin.ACS chemical neuroscience · 2022Article
- Siah-1-interacting protein regulates mutated huntingtin protein aggregation in Huntington's disease models.Cell & bioscience · 2022Article
- Review
- Decreased Interactions between Calmodulin and a Mutant Huntingtin Model Might Reduce the Cytotoxic Level of Intracellular CaInternational journal of molecular sciences · 2021Article
- Targeting microglia L-type voltage-dependent calcium channels for the treatment of central nervous system disorders.Journal of neuroscience research · 2021Review
- BACHD Mice Recapitulate the Striatal Parvalbuminergic Interneuron Loss Found in Huntington's Disease.Frontiers in neuroanatomy · 2021Article
- Molecular Components of Store-Operated Calcium Channels in the Regulation of Neural Stem Cell Physiology, Neurogenesis, and the Pathology of Huntington's Disease.Frontiers in cell and developmental biology · 2021Review
- STIM2 Mediates Excessive Store-Operated Calcium Entry in Patient-Specific iPSC-Derived Neurons Modeling a Juvenile Form of Huntington's Disease.Frontiers in cell and developmental biology · 2021Article
- Article
- Calcium-Handling Defects and Neurodegenerative Disease.Cold Spring Harbor perspectives in biology · 2020Review
- S100A6 and Its Brain Ligands in Neurodegenerative Disorders.International journal of molecular sciences · 2020Review
- Dysregulation of Neuronal Calcium Signaling via Store-Operated Channels in Huntington's Disease.Frontiers in cell and developmental biology · 2020Review
- STIM Proteins and Glutamate Receptors in Neurons: Role in Neuronal Physiology and Neurodegenerative Diseases.International journal of molecular sciences · 2019Review
- Polyelectrolyte membrane scaffold sustains growth of neuronal cells.Journal of biomedical materials research. Part A · 2019Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's disease (HD) is a hereditary neurodegenerative disease caused by the expansion of a polyglutamine stretch in the huntingtin (HTT) protein and characterized by dysregulated calcium homeostasis. We investigated whether these disturbances are correlated with changes in the mRNA level of the genes that encode proteins involved in calcium homeostasis and signaling (i.e., the calciosome). Using custom-made TaqMan low-density arrays containing probes for 96 genes, we quantified mRNA in the striatum in YAC128 mice, a model of HD, and wildtype mice. HTT mutation caused the increased expression of some components of the calcium signalosome, including calretinin, presenilin 2, and calmyrin 1, and the increased expression of genes indirectly involved in calcium homeostasis, such as huntingtin-associated protein 1 and calcyclin-binding protein. To verify these findings in a different model, we used PC12 cells with an inducible expression of mutated full-length HTT. Using single-cell imaging with Fura-2AM, we found that store-operated Ca(2+) entry but not endoplasmic reticulum (ER) store content was changed as a result of the expression of mutant HTT. Statistically significant downregulation of the Orai calcium channel subunit 2, calmodulin, and septin 4 was detected in cells that expressed mutated HTT. Our data indicate that the dysregulation of calcium homeostasis correlates with changes in the gene expression of members of the calciosome. These changes, however, differed in the two models of HD used in this study. Our results indicate that each HD model exhibits distinct features that may only partially resemble the human disease.
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