ArticleFEBS open bio2020
A mouse model of Timothy syndrome exhibits altered social competitive dominance and inhibitory neuron development.
Article in FEBS open bio, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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
12 citing papers in PubMed, 19 citations in OpenAlex.
- Article
- Operant House: A versatile open-source platform for automated operant conditioning testing of mice in home cages.PloS one · 2026Article
- Animal models of autism spectrum disorder: Insights into genetic, structural and environmental models.Veterinarni medicina · 2025Review
- Disruptions in primary visual cortex physiology and function in a mouse model of Timothy syndrome.Cerebral cortex (New York, N.Y. : 1991) · 2025Article
- Automated Behavioral Analysis of Schizophrenia-like Phenotypes in Repeated MK-801-Treated Mice Using IntelliCage.International journal of molecular sciences · 2025Article
- Synaptic plasticity deficits in a mouse model of Timothy syndrome: LTP saturation and its pharmacological rescue by nifedipine.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Article
- Cognitive Impairment and Synaptic Dysfunction in Cardiovascular Disorders: The New Frontiers of the Heart-Brain Axis.Biomedicines · 2024Review
- L-type calcium channels and neuropsychiatric diseases: Insights into genetic risk variant-associated genomic regulation and impact on brain development.Channels (Austin, Tex.) · 2023Review
- IntelliCage: the development and perspectives of a mouse- and user-friendly automated behavioral test system.Frontiers in behavioral neuroscience · 2023Review
- The CaNeuropharmacology · 2022Article
- Identification of ultra-rare disruptive variants in voltage-gated calcium channel-encoding genes in Japanese samples of schizophrenia and autism spectrum disorder.Translational psychiatry · 2022Article
- Loss of Cav1.2 channels impairs hippocampal theta burst stimulation-induced long-term potentiation.Channels (Austin, Tex.) · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple genetic factors related to autism spectrum disorder (ASD) have been identified, but the biological mechanisms remain obscure. Timothy syndrome (TS), associated with syndromic ASD, is caused by a gain-of-function mutation, G406R, in the pore-forming subunit of L-type 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.