ArticleActa epileptologica2024
Revealing the complex role of CDKL5 in developmental epilepsy through a calcium channel related vision.
Article in Acta epileptologica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- CDKL5 Deficiency Disorder: Revealing the Molecular Mechanism of Pathogenic Variants.International journal of molecular sciences · 2025Article
- Adult-Onset Deletion of CDKL5 in Forebrain Glutamatergic Neurons Impairs Synaptic Integrity and Behavior in Mice.International journal of molecular sciences · 2025Article
Corrections and comments
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3 authors.
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Abstract
Developmental and epileptic encephalopathies are severe neurological conditions in clinical practice, among which loss-of-function mutations in brain-enriched serine-threonine kinase cyclin dependent kinase like-5 (CDKL5) exists as one of the most common types. It is unknown, therefore, how precisely CDKL5 mutations lead to neuronal hyper-excitation. A recent study that looked at the connection between voltage-gated calcium channel Cav2.3 and CDKL5 in an experimental context was published in Nature Communications. This study has revealed that Cav2.3, a physiological phosphorylation target of CDKL5, would show delayed inactivation and increased cholinergic stimulation in CDKL5 knock out conditions. This would in turn cause neuronal hyperexcitability and related enhanced seizure susceptibility. This work, in our opinion, provided fresh insight into the epileptic encephalopathies linked to CDKL5 and highlighted Cav2.3 as a possible target for it.
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