ArticleMolecular autism2020
Biophysical classification of a
Article in Molecular autism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- Calcium channelopathies and intellectual disability: a systematic review.Orphanet journal of rare diseases · 2021Pooled it
- Identification of novel functional sites in the CaProceedings of the National Academy of Sciences of the United States of America · 2026Article
- PRMT5-Cacna1d axis maintains calcium homeostasis to regulate postnatal motor development in mice.Cellular and molecular life sciences : CMLS · 2026Article
- Whole-exome sequencing in children with dyslexia implicates rare variants in CLDN3 and ion channel genes.Human genetics · 2025Article
- Quantitative Proteomics Identifies Potential Molecular Adaptations in Mouse Models of Congenital Stationary Night Blindness Type 2.Molecular & cellular proteomics : MCP · 2025Article
- Inactivation of CaV1 and CaV2 channels.The Journal of general physiology · 2025Review
- A structural analysis of the splice-specific functional impact of the pathogenic familial hemiplegic migraine type 1 S218L mutation on CaMolecular brain · 2024Article
- The L-type calcium channel CaV1.3: A potential target for cancer therapy.Journal of cellular and molecular medicine · 2024Review
- A Novel De Novo Gain-of-FunctionNeurology. Genetics · 2024Article
- Pathogenicity of de novo CACNA1D CaEuropean journal of human genetics : EJHG · 2024Article
- Shared genetic basis connects smoking behaviors and bone health: insights from a genome-wide cross-trait analysis.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024Article
- Characterization of two pathological gating-charge substitutions in Cav1.4 L-type calcium channels.Channels (Austin, Tex.) · 2023Article
- L-type calcium channels and neuropsychiatric diseases: Insights into genetic risk variant-associated genomic regulation and impact on brain development.Channels (Austin, Tex.) · 2023Review
- Germline de novo variant F747S extends the phenotypic spectrum of CACNA1D Ca2+ channelopathies.Human molecular genetics · 2023Article
- Case Report: Clinical delineation ofFrontiers in neurology · 2023Article
- CACNA1D-Related Channelopathies: From Hypertension to Autism.Handbook of experimental pharmacology · 2023Review
- Impaired CaJournal of molecular and cellular cardiology · 2022Article
- Whole Exome Sequencing Identifies a Heterozygous Variant in the Cav1.3 GeneInternational journal of molecular sciences · 2022Article
- Calcium signaling in neurodevelopment and pathophysiology of autism spectrum disorders.Molecular biology reports · 2022Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Background: There is increasing evidence that de novo Methods: For functional characterization, wild-type and mutant Cav1.3 channel complexes were expressed in tsA-201 cells and tested for typical gain-of-function gating changes using the whole-cell patch-clamp technique. Results: Mutation S652L significantly shifted the voltage-dependence of activation and steady-state inactivation to more negative potentials (~ 13-17 mV) and increased window currents at subthreshold voltages. Moreover, it slowed tail currents and increased Ca
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.