Evidence map›Paper›PMID 34370157›Full record

ArticleNeurogenetics2021

Clinical and genetic analysis of six Chinese children with Poirier-Bienvenu neurodevelopmental syndrome caused by CSNK2B mutation.

Sai Yang, Liwen Wu, Hongmei Liao, Xiulan Lu, Xiao Zhang, Xiaojun Kuang, Liming Yang

Abstract read
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In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.3field-weighted citation impact, top 12% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. A recurrentBiochemistry and biophysics reports · 2026
    Article
  3. Article
  4. Article
  5. CSNK2B Mutation: A Rare Cause of IGHD.Clinical endocrinology · 2025
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. HGG advances · 2022
    Article
  11. Review
  12. Article
  13. Predictive functional, statistical and structural analysis ofFrontiers in molecular biosciences · 2022
    Article
  14. Splicing Interruption by Intron Variants inFrontiers in neuroscience · 2022
    Article
  15. Frontiers in neurology · 2022
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Sai YangDepartment of Neurology, Hunan Children's Hospital, Ziyuan Road & No. 86, Changsha, 410001, Hunan, China.
Liwen WuDepartment of Neurology, Hunan Children's Hospital, Ziyuan Road & No. 86, Changsha, 410001, Hunan, China.
Hongmei LiaoDepartment of Neurology, Hunan Children's Hospital, Ziyuan Road & No. 86, Changsha, 410001, Hunan, China.
Xiulan LuDepartment of Neurology, Hunan Children's Hospital, Ziyuan Road & No. 86, Changsha, 410001, Hunan, China.
Xiao ZhangDepartment of Neurology, Hunan Children's Hospital, Ziyuan Road & No. 86, Changsha, 410001, Hunan, China.
Xiaojun KuangDepartment of Neurology, Hunan Children's Hospital, Ziyuan Road & No. 86, Changsha, 410001, Hunan, China.
Liming YangDepartment of Neurology, Hunan Children's Hospital, Ziyuan Road & No. 86, Changsha, 410001, Hunan, China. liming_yang01@163.com.
Hunan Children's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

PhenotypeAsian PeopleCasein Kinase IIChild, PreschoolCohort StudiesDevelopmental DisabilitiesExome SequencingFemaleGenetic TestingHumansInfantInfant, NewbornIntellectual DisabilityMaleMutationNeurodevelopmental DisordersCasein Kinase IICasein kinase 2CSNK2BIntellectual disabilitySeizures

Identifiers

PMID34370157
OpenAlexW3190474812

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.