| Literature DB >> 33025479 |
Guiyu Lou1,2,3, Yang Ke1,2,3, Yuwei Zhang1,2,3, Guo Liangjie1,2,3, Samaa Abdelmonem Shama4, Na Qi1,2,3, Litao Qin1,2,3, Shixiu Liao5,6,7, Yuanyin Zhao8.
Abstract
Cohen syndrome (CS) is an autosomal recessive congenital disorder characterized by mutation in the vacuolar protein sorting 13 homolog B (VPS13B; formerly COH1) gene. In the current study, a Chinese family has two young sibling cases having a developmental delay, physical obesity, high myopia, and a special face, which suspected to be CS. The purpose of the study was to identify variants and further analyze their pathogenicity for CS. Next-generation sequencing (NGS) revealed a compound heterozygous mutation in VPS13B gene in the proband, which comprises a frameshift mutation in NM_017890.4: c.10076_10077delCA (p.T3359fs*29) and a putative splice site mutation in c.6940 + 1G > T. Both Minigene assay in vitro and splicing assay in vivo confirmed that the splicing mutation in c.6940 + 1G > T generates a frameshift transcript with whole exon 38 skipping. Eventually, quantitative real-time PCR demonstrated that either of the two mutations can lead to degradation of the VPS13B gene at the transcriptional level. Functional studies of variants identified in CS patients are essential for their subsequent genetic counseling and prenatal diagnoses and could also be the start point for new therapeutic approaches, currently based only on symptomatic treatment.Entities:
Keywords: Cohen syndrome; Functional analysis; Mutation; Pedigree; VPS13B gene
Year: 2020 PMID: 33025479 DOI: 10.1007/s12031-020-01713-6
Source DB: PubMed Journal: J Mol Neurosci ISSN: 0895-8696 Impact factor: 3.444