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CHL1基因杂合缺失:1例新病例的详细阵列比较基因组杂交及临床特征分析并文献复习

Heterozygous deletion of CHL1 gene: detailed array-CGH and clinical characterization of a new case and review of the literature.

作者信息

Tassano Elisa, Biancheri Roberta, Denegri Laura, Porta Simona, Novara Francesca, Zuffardi Orsetta, Gimelli Giorgio, Cuoco Cristina

出版信息

Eur J Med Genet. 2014 Nov-Dec;57(11-12):626-9. doi: 10.1016/j.ejmg.2014.09.007.

Abstract

CHL1 gene maps at 3p26.3 and encodes a cell adhesion molecule of the immunoglobulin superfamily highly expressed in the brain. CHL1 regulates neuronal migration and neurite overgrowth in the developing brain, while in mature neurons it accumulates in the axonal membrane and regulates synapse function via the clathrin-dependent pathways. To our knowledge, to date only three familial cases presenting heterozygous deletion of chromosome 3 at band p26.3, including only the CHL1 gene, have been reported. All the patients presented cognitive impairment characterized by learning and language difficulties. Here, we describe a six-year-old boy in which array-CGH analysis disclosed a terminal 3p26.3 deletion. The deletion was transmitted from his normal mother and included only the CHL1 gene. Our patient presented microcephaly, short stature, mild mental retardation, learning and language delay, and strabismus. In our study we compare the phenotypic and molecular cytogenetic features of CHL1 gene deletion cases. Verbal function developmental delay seems to be a common key finding. The concomitance of the genetic and phenotypic alterations could be a good evidence of a new emerging syndrome associated with the deletion of CHL1 gene alone, although the identification of new cases is required.

摘要

CHL1基因定位于3p26.3,编码一种免疫球蛋白超家族的细胞粘附分子,在脑中高度表达。CHL1在发育中的大脑中调节神经元迁移和神经突过度生长,而在成熟神经元中,它聚集在轴突膜中,并通过网格蛋白依赖途径调节突触功能。据我们所知,迄今为止仅报道了3例家族性病例,其3号染色体p26.3带存在杂合性缺失,且仅涉及CHL1基因。所有患者均表现出以学习和语言困难为特征的认知障碍。在此,我们描述了一名6岁男孩,其通过阵列比较基因组杂交分析发现存在3p26.3末端缺失。该缺失由其正常母亲遗传而来,且仅包含CHL1基因。我们的患者表现为小头畸形、身材矮小、轻度智力发育迟缓、学习和语言发育延迟以及斜视。在我们的研究中,我们比较了CHL1基因缺失病例的表型和分子细胞遗传学特征。语言功能发育延迟似乎是一个常见的关键发现。遗传和表型改变的同时出现可能是一种仅与CHL1基因缺失相关的新兴综合征的有力证据,尽管还需要发现新的病例。

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