Literature DB >> 33358638

A de novo CHD3 variant in a child with intellectual disability, autism, joint laxity, and dysmorphisms.

Miyako Mizukami1, Aki Ishikawa2, Sachiko Miyazaki2, Akiko Tsuzuki3, Sakae Saito4, Tetsuya Niihori5, Akihiro Sakurai2.   

Abstract

BACKGROUND: Chromodomain helicase DNA-binding (CHD) proteins play important roles in developmental processes. CHD3, a member of the CHD family of proteins, was reported to be a cause of a neurodevelopmental syndrome by Snijders Blok et al., but only a small number of probands have been reported. CASE REPORT: The patient was a 9-year-old female with severe intellectual disability, speech impairment, autism, joint laxity and dysmorphisms. Whole exome sequencing revealed a de novo missense variant in CHD3 (NM_001005273:exon18: c.2896C > T:p.R966W).
CONCLUSION: We report a case with a pathogenic variant in the CHD3 gene. Our report indicates that CHD3 analysis is helpful for diagnosis of the cases with neurodevelopmental disorders, joint laxity, and coarse facial phenotype.
Copyright © 2020 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved.

Entities:  

Keywords:  CHD3; Dysmorphisms; Intellectual disability; Joint laxity; Snijders Blok-Campeau syndrome; Speech delay

Year:  2020        PMID: 33358638     DOI: 10.1016/j.braindev.2020.12.004

Source DB:  PubMed          Journal:  Brain Dev        ISSN: 0387-7604            Impact factor:   1.961


  1 in total

1.  Snijders Blok-Campeau syndrome caused by CHD3 gene mutation: a case report.

Authors:  Xi-Yong Fan
Journal:  Zhongguo Dang Dai Er Ke Za Zhi       Date:  2021 Sept 15
  1 in total

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