ReviewPflugers Archiv : European journal of physiology2010
CaV2.1 channelopathies.
Review in Pflugers Archiv : European journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
125 citing papers in PubMed, 211 citations in OpenAlex.
- Tiered modelling of a CACNA1A D1634N mutation linked to ataxia, epilepsy and cognitive deficits.Brain : a journal of neurology · 2026Article
- Investigating genetic susceptibility to concussion through rare variants in ion channel and neurotransmission genes.Journal of neurology · 2026Article
- Calmodulinopathy variants impair CaV1.3 and CaV2.1 regulation.The Journal of general physiology · 2026Article
- Genotype and Age at Onset Drive Vermis Atrophy in CACNA1A- and GAA-FGF14-related Ataxias.Cerebellum (London, England) · 2026Article
- Intellectual disability and structural defects of the CaV2.1 channel in episodic ataxia type 2: correlation using an AI prediction model.Journal of neurology · 2026Article
- Article
- Case Report: Thymoma-associated stiff person syndrome and myasthenia gravis: an index case with exploratory exome sequencing and review of reported cases.Frontiers in oncology · 2026Article
- Unveiling β Subunit-Dependent Gating Defects in CaNeuroscience bulletin · 2026Article
- Cerebellar Micro Complex Model Using Histologic Boolean Mapping Simulates Adaptive Motor Control.Neuroinformatics · 2025Article
- A rich conformational palette underlies human CaNature communications · 2025Article
- Is migraine a common manifestation of CADASIL? Arguments Pros.The journal of headache and pain · 2025Article
- Prolonged apnea in a boy with epilepsy and a novel gain-of-function missense CACNA1A variant indicating SUDEP risk.Frontiers in neurology · 2025Article
- Calcium Ions in the Physiology and Pathology of the Central Nervous System.International journal of molecular sciences · 2024Review
- Pin1 promotes human CaCell communication and signaling : CCS · 2024Article
- Structural basis for different ω-agatoxin IVA sensitivities of the P-type and Q-type CaCell research · 2024Article
- The clinical utility and diagnostic implementation of human subject cell transdifferentiation followed by RNA sequencing.American journal of human genetics · 2024Article
- The Interplay Between Splicing of Two Exon Combinations Differentially Affects Membrane Targeting and Function of Human CaFunction (Oxford, England) · 2024Article
- Clinical and electrophysiological features of SCN8A variants causing episodic or chronic ataxia.EBioMedicine · 2023Article
- Early molecular layer interneuron hyperactivity triggers Purkinje neuron degeneration in SCA1.Neuron · 2023Article
- Identification of Dp140 and α1-syntrophin as novel molecular interactors of the neuronal CaPflugers Archiv : European journal of physiology · 2023Article
65 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Mutations in the CACNA1A gene that encodes the pore-forming alpha1 subunit of human voltage-gated CaV2.1 (P/Q-type) Ca2+ channels cause several autosomal-dominant neurologic disorders, including familial hemiplegic migraine type 1 (FHM1), episodic ataxia type 2, and spinocerebellar ataxia type 6 (SCA6). For each channelopathy, the review describes the disease phenotype as well as the functional consequences of the disease-causing mutations on recombinant human CaV2.1 channels and, in the case of FHM1 and SCA6, on neuronal CaV2.1 channels expressed at the endogenous physiological level in knockin mouse models. The effects of FHM1 mutations on cortical spreading depression, the phenomenon underlying migraine aura, and on cortical excitatory and inhibitory synaptic transmission in FHM1 knockin mice are also described, and their implications for the disease mechanism discussed. Moreover, the review describes different ataxic spontaneous cacna1a mouse mutants and the important insights into the cerebellar mechanisms underlying motor dysfunction caused by mutant CaV2.1 channels that were obtained from their functional characterization.
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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.