ArticleNeurogenetics2021
Clinical and genetic analysis of six Chinese children with Poirier-Bienvenu neurodevelopmental syndrome caused by CSNK2B mutation.
Article in Neurogenetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 16 citations in OpenAlex.
- CSNK2B-associated epilepsy: family report and literature review.Acta epileptologica · 2026Article
- A recurrentBiochemistry and biophysics reports · 2026Article
- CSNK2B gene replacement rescues autism-related phenotypes and establishes translational EEG biomarkers.Cell reports. Medicine · 2026Article
- Genetic analysis of four cases of Poirier Bienvenu neurodevelopmental syndrome associated with CSNK2B variant.BMC medical genomics · 2025Article
- CSNK2B Mutation: A Rare Cause of IGHD.Clinical endocrinology · 2025Article
- Case Report: A case of Poirier-Bienvenu neurodevelopmental syndrome manifesting primarily as eyelid myoclonia.Frontiers in pediatrics · 2025Article
- Casein Kinase 2 Affects Epilepsy by Regulating Ion Channels: A Potential Mechanism.CNS & neurological disorders drug targets · 2024Review
- Analyzing the interactome of human CK2β in prostate carcinoma cells reveals HSP70-1 and Rho guanin nucleotide exchange factor 12 as novel interaction partners.FASEB bioAdvances · 2023Article
- Case report: Two cases of Poirier-Bienvenu neurodevelopmental syndrome and review of literature.Frontiers in pediatrics · 2023Article
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- Review
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- Predictive functional, statistical and structural analysis ofFrontiers in molecular biosciences · 2022Article
- Splicing Interruption by Intron Variants inFrontiers in neuroscience · 2022Article
- Article
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Authors and funding
7 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Mutations in CSNK2B lead to Poirier-Bienvenu neurodevelopmental syndrome (POBINDS), a rare neurodevelopmental disorder. Only 14 cases of POBINDS have been reported worldwide. The main manifestations are seizures, often tonic-clonic, with or without intellectual disability, growth retardation, and developmental language retardation. We conducted a comprehensive phenotypic mining and trio-whole exome sequencing on six children with POBINDS for gene diagnosis and analyzed the different variants using bioinformatics analysis software and related experiments. This paper reviews previous literature and discusses two common missense variants that lead to structural changes. Among the six patients, four, one, and one had tonic-clonic, myoclonic, and febrile seizures, respectively. Language development disorder, motor development disorder, and developmental delay/intellectual disability (DD/ID) are the main clinical features. All children had de novo mutations in CSNK2B, including three missense variants (c.410G > T/p.(Cys137Phe), c.494A > G/p.(His165Arg), and c.3G > A/p.(Met1Ile)), two splice variants (c.292-2A > T, c.558-3 T > G), and one frameshift variant (c.499delC/p.(Leu167Serfs*60)). Three missense variants were predicted to be harmful by various software programs, and two splicing variants were found to produce new exonic splicing enhancers by the minigene assay. Western blot analysis showed that the frameshift variant resulted in decreased protein expression. According to a literature review, c.3G > A/p.(Met1Ile), c.292-2A > T, c.558-3 T > G, and c.499delC/p.(Leu167Serfs*60) are novel variants of CSNK2B. The decrease or loss of protein function caused by CSNK2B mutations may be a pathogenic factor in this cohort. The severity of the POBINDS phenotype differs, and refractory epilepsy may be accompanied by a more serious DD/ID, language disorder, and motor retardation. At present, there is no specific treatment, and antiepileptic therapy usually requires the combination of two or more anti-epileptic drugs.
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