ArticleBrain communications2022
A rat model of a focal mosaic expression of PCDH19 replicates human brain developmental abnormalities and behaviours.
Article in Brain communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- Rodent models of genetic epilepsy and its association with neurocognitive impairment- a systematic review.Frontiers in pharmacology · 2025Pooled it
- Canalization of neural dynamics by δ-protocadherins in the developing zebrafish optic tectum.PLoS genetics · 2026Article
- Bidirectional interaction between protocadherin 8 and the transcription factor Dbx1 regulates cerebral cortex development.Development (Cambridge, England) · 2026Article
- Proteomic analysis of the developing mammalian brain links PCDH19 to the Wnt/β-catenin signalling pathway.Molecular psychiatry · 2024Article
- Altered cytoskeleton dynamics in patient-derived iPSC-based model of PCDH19 clustering epilepsy.Frontiers in cell and developmental biology · 2024Article
- Optogenetic and chemogenetic manipulation of seizure threshold in mice.STAR protocols · 2023Article
- Genetic variants and phenotype analysis in a five-generation Chinese pedigree withFrontiers in neurology · 2023Article
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Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protocadherin 19 gene-related epilepsy or protocadherin 19 clustering epilepsy is an infantile-onset epilepsy syndrome characterized by psychiatric (including autism-related), sensory, and cognitive impairment of varying degrees. Protocadherin 19 clustering epilepsy is caused by X-linked protocadherin 19 protein loss of function. Due to random X-chromosome inactivation, protocadherin 19 clustering epilepsy-affected females present a mosaic population of healthy and protocadherin 19-mutant cells. Unfortunately, to date, no current mouse model can fully recapitulate both the brain histological and behavioural deficits present in people with protocadherin 19 clustering epilepsy. Thus, the search for a proper understanding of the disease and possible future treatment is hampered. By inducing a focal mosaicism of protocadherin 19 expression using
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Registered trials
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