ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
Neuroprotective effects of inositol 1,4,5-trisphosphate receptor C-terminal fragment in a Huntington's disease mouse model.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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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.
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Who cites it
56 citing papers in PubMed, 90 citations in OpenAlex.
- Calcium Signalling in Neurological Disorders, with Insights from Miniature Fluorescence Microscopy.Cells · 2024Review
- Calcium Ions in the Physiology and Pathology of the Central Nervous System.International journal of molecular sciences · 2024Review
- Axonal ER CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Small-Molecule Disruptors of Mutant Huntingtin-Calmodulin Protein-Protein Interaction Attenuate Deleterious Effects of Mutant Huntingtin.ACS chemical neuroscience · 2022Article
- Inflammation and Nitro-oxidative Stress as Drivers of Endocannabinoid System Aberrations in Mood Disorders and Schizophrenia.Molecular neurobiology · 2022Review
- Purinergic Receptors in Basal Ganglia Diseases: Shared Molecular Mechanisms between Huntington's and Parkinson's Disease.Neuroscience bulletin · 2020Review
- Inositol 1,4,5-Trisphosphate Receptors in Human Disease: A Comprehensive Update.Journal of clinical medicine · 2020Review
- Dysregulation of Neuronal Calcium Signaling via Store-Operated Channels in Huntington's Disease.Frontiers in cell and developmental biology · 2020Review
- Bi-allelic variants in RNF170 are associated with hereditary spastic paraplegia.Nature communications · 2019Article
- Review
- Neuronal Sigma-1 Receptors: Signaling Functions and Protective Roles in Neurodegenerative Diseases.Frontiers in neuroscience · 2019Review
- Article
- Cause or compensation?-Altered neuronal CaCNS neuroscience & therapeutics · 2018Review
- Calcium signaling and molecular mechanisms underlying neurodegenerative diseases.Cell calcium · 2018Review
- On the Role of Store-Operated Calcium Entry in Acute and Chronic Neurodegenerative Diseases.Frontiers in molecular neuroscience · 2018Review
- Inhibition of TRPC1-Dependent Store-Operated Calcium Entry Improves Synaptic Stability and Motor Performance in a Mouse Model of Huntington's Disease.Journal of Huntington's disease · 2018Article
- Determining the Roles of Inositol Trisphosphate Receptors in Neurodegeneration: Interdisciplinary Perspectives on a Complex Topic.Molecular neurobiology · 2017Review
- The sigma-1 receptor mediates the beneficial effects of pridopidine in a mouse model of Huntington disease.Neurobiology of disease · 2017Article
- The entangled ER-mitochondrial axis as a potential therapeutic strategy in neurodegeneration: A tangled duo unchained.Cell calcium · 2016Review
- Enhanced Store-Operated Calcium Entry Leads to Striatal Synaptic Loss in a Huntington's Disease Mouse Model.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Huntington's disease (HD) is a dominantly inherited, progressive neurodegenerative disease caused by an expanded polyglutamine tract in huntingtin protein (Htt). Medium spiny striatal neurons (MSNs) are primarily affected in HD. Mutant huntingtin protein (Htt(exp)) specifically binds to and activates type 1 inositol 1,4,5-trisphosphate receptor (InsP(3)R1), an intracellular Ca(2+) release channel. Htt(exp)-InsP(3)R1 association is mediated by a cytosolic C-terminal tail of InsP(3)R1 (a 122-aa-long IC10 fragment). To evaluate an importance of Htt(exp) association with InsP(3)R1 for HD pathology, we generated lentiviral and adeno-associated viruses expressing GFP-IC10 fusion protein and performed a series of experiments with YAC128 HD transgenic mouse. Infection with Lenti-GFP-IC10 virus stabilized Ca(2+) signaling in cultured YAC128 MSNs and protected YAC128 MSNs from glutamate-induced apoptosis. Intrastriatal injections of AAV1-GFP-IC10 significantly alleviated motor deficits and reduced MSN loss and shrinkage in YAC128 mice. Our results demonstrate an importance of InsP(3)R1-Htt(exp) association for HD pathogenesis and suggested that InsP(3)R1 is a potential therapeutic target for HD. Our data also support potential use of IC10 peptide as a novel HD therapeutic agent.
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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.