ArticleTranslational psychiatry2015
Shared functional defect in IP₃R-mediated calcium signaling in diverse monogenic autism syndromes.
Article in Translational psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Genetic associations between voltage-gated calcium channels and autism spectrum disorder: a systematic review.Molecular brain · 2020Pooled it
- Mitochondria-ER contact sites in neurological disorders.Animal cells and systems · 2026Review
- From spatial patterning to coordinated execution: a cross-system framework for autism spectrum disorder.Frontiers in psychiatry · 2026Review
- Behavioral and molecular insights into anxiety in ube3a and fmr1 zebrafish models of autism spectrum disorders.Translational psychiatry · 2025Article
- Article
- Review
- Ginsenoside Rh3-induced neurotoxicity involving the IP3R-CaJournal of natural medicines · 2025Article
- Gangliosides and Cholesterol: Dual Regulators of Neuronal Membrane Framework in Autism Spectrum Disorder.International journal of molecular sciences · 2025Review
- Whole Genome Analysis of Dizygotic Twins With Autism Reveals Prevalent Transposon Insertion Within Neuronal Regulatory Elements: Potential Implications for Disease Etiology and Clinical Assessment.Journal of autism and developmental disorders · 2023Article
- Insights into the role of intracellular calcium signaling in the neurobiology of neurodevelopmental disorders.Frontiers in neuroscience · 2023Review
- Calcium signaling in neurodevelopment and pathophysiology of autism spectrum disorders.Molecular biology reports · 2022Review
- Calcium and activity-dependent signaling in the developing cerebral cortex.Development (Cambridge, England) · 2022Review
- Caspr2 interacts with type 1 inositol 1,4,5-trisphosphate receptor in the developing cerebellum and regulates Purkinje cell morphology.The Journal of biological chemistry · 2020Article
- Inositol 1,4,5-Trisphosphate Receptors in Human Disease: A Comprehensive Update.Journal of clinical medicine · 2020Review
- Coupling of autism genes to tissue-wide expression and dysfunction of synapse, calcium signalling and transcriptional regulation.PloS one · 2020Article
- Review
- Spatial-temporal patterning of CaSeminars in cell & developmental biology · 2019Review
- Applying Deep Neural Network Analysis to High-Content Image-Based Assays.SLAS discovery : advancing life sciences R & D · 2019Article
- STIM1 Is Required for Remodeling of the Endoplasmic Reticulum and Microtubule Cytoskeleton in Steering Growth Cones.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- All three IPScience signaling · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Autism spectrum disorder (ASD) affects 2% of children, and is characterized by impaired social and communication skills together with repetitive, stereotypic behavior. The pathophysiology of ASD is complex due to genetic and environmental heterogeneity, complicating the development of therapies and making diagnosis challenging. Growing genetic evidence supports a role of disrupted Ca(2+) signaling in ASD. Here, we report that patient-derived fibroblasts from three monogenic models of ASD-fragile X and tuberous sclerosis TSC1 and TSC2 syndromes-display depressed Ca(2+) release through inositol trisphosphate receptors (IP3Rs). This was apparent in Ca(2+) signals evoked by G protein-coupled receptors and by photoreleased IP3 at the levels of both global and local elementary Ca(2+) events, suggesting fundamental defects in IP3R channel activity in ASD. Given the ubiquitous involvement of IP3R-mediated Ca(2+) signaling in neuronal excitability, synaptic plasticity, gene expression and neurodevelopment, we propose dysregulated IP3R signaling as a nexus where genes altered in ASD converge to exert their deleterious effect. These findings highlight potential pharmaceutical targets, and identify Ca(2+) screening in skin fibroblasts as a promising technique for early detection of individuals susceptible to ASD.
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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 Socratic graph.