ArticleNeuron2019
α1ACT Is Essential for Survival and Early Cerebellar Programming in a Critical Neonatal Window.
Article in Neuron, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- Calcium channelopathies and intellectual disability: a systematic review.Orphanet journal of rare diseases · 2021Pooled it
- Mitochondrial and lysosomal dysfunctions might be involved in the pathogenesis of the CACNA1A-related neurodevelopmental disorders according to in vitro studies.Biological research · 2025Article
- Resting-State EEG Analysis Characterizes the Signature of CACNA1A-and GAA-FGF14-Related Channelopathies.Cerebellum (London, England) · 2025Article
- CACNA1A loss-of-function affects neurogenesis in human iPSC-derived neural models.Cellular and molecular life sciences : CMLS · 2025Article
- Calcium channel-coupled transcription factors facilitate direct nuclear signaling.Research square · 2025Article
- Article
- Insights on the Shared Genetic Landscape of Neurodevelopmental and Movement Disorders.Current neurology and neuroscience reports · 2025Review
- Pancreatic β cell-secreted factor FGF23 attenuates Alzheimer's disease-related amyloid β-induced neuronal death.PNAS nexus · 2025Article
- The Role of Protein Quantity Control in Polyglutamine Spinocerebellar Ataxias.Cerebellum (London, England) · 2024Review
- Evaluation of histological and ultrastructural changes provoked by prenatal tramadol on postnatal cortical cerebellar neuronal development in rats: possible implication of Ki67, GFAP and MicroRNA-7/P53 signalling trajectories.Journal of molecular histology · 2024Article
- Novel de novo heterozygous CACNA1A gene variant in generalised dystonia: a case report.BMJ neurology open · 2024Article
- Endosomal dysfunction contributes to cerebellar deficits in spinocerebellar ataxia type 6.eLife · 2023Article
- Functional implications of paralog genes in polyglutamine spinocerebellar ataxias.Human genetics · 2023Review
- The Transcription Factor, α1ACT, Acts Through a MicroRNA Network to Regulate Neurogenesis and Cell Death During Neonatal Cerebellar Development.Cerebellum (London, England) · 2023Article
- Overexpression of the autism candidate geneFrontiers in cellular neuroscience · 2023Article
- CACNA1A-Related Channelopathies: Clinical Manifestations and Treatment Options.Handbook of experimental pharmacology · 2023Review
- HER2 c-Terminal Fragments Are Expressed via Internal Translation of the HER2 mRNA.International journal of molecular sciences · 2022Article
- Cytosolic peptides encoding CaCommunications biology · 2022Article
- More than a pore: How voltage-gated calcium channels act on different levels of neuronal communication regulation.Channels (Austin, Tex.) · 2021Review
- Commentary to: "The Pathophysiology and Clinical Manifestations of Spinocerebellar Ataxia Type 6" by Rentiya et al., Cerebellum 2020;19(3):459-464).Cerebellum (London, England) · 2021Article
Corrections and comments
- Commented on by
Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Postnatal cerebellar development is a precisely regulated process involving well-orchestrated expression of neural genes. Neurological phenotypes associated with CACNA1A gene defects have been increasingly recognized, yet the molecular principles underlying this association remain elusive. By characterizing a dose-dependent CACNA1A gene deficiency mouse model, we discovered that α1ACT, as a transcription factor and secondary protein of CACNA1A mRNA, drives dynamic gene expression networks within cerebellar Purkinje cells and is indispensable for neonatal survival. Perinatal loss of α1ACT leads to motor dysfunction through disruption of neurogenesis and synaptic regulatory networks. However, its elimination in adulthood has minimal effect on the cerebellum. These findings shed light on the critical role of α1ACT in facilitating neuronal development in both mice and humans and support a rationale for gene therapies for calcium-channel-associated cerebellar disorders. Finally, we show that bicistronic expression may be common to the voltage-gated calcium channel (VGCC) gene family and may help explain complex genetic syndromes.
Indexed as
Identifiers
What OpenQuestion holds
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.