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一种新的17q21.33区域1.8 Mb新发微缺失,与智力残疾和畸形特征相关。

A novel de novo 1.8 Mb microdeletion of 17q21.33 associated with intellectual disability and dysmorphic features.

作者信息

Preiksaitiene E, Männik K, Dirse V, Utkus A, Ciuladaite Z, Kasnauskiene J, Kurg A, Kučinskas V

机构信息

Department of Human and Medical Genetics, Faculty of Medicine, Vilnius University, Vilnius, Lithuania.

出版信息

Eur J Med Genet. 2012 Nov;55(11):656-9. doi: 10.1016/j.ejmg.2012.07.008. Epub 2012 Jul 27.

Abstract

We report on a de novo 17q21.33 microdeletion, 1.8 Mb in size, detected in a patient with mild intellectual disability, growth retardation, poor weight gain, microcephaly, long face, large beaked nose, thick lower lip, micrognathia and other dysmorphic features. The deletion was detected by whole-genome genotyping BeadChip assay and involves the genomic region between 45,682,246 and 47,544,816 bp on chromosome 17. Among the 24 RefSeq genes included in this deletion are the CA10 and CACNA1G genes that are involved in brain development and neurological processes. A possible candidate gene for the prenatal and postnatal growth retardation is the CHAD gene, which product chondroadherin is a cartilage protein with cell binding properties. These three genes may be responsible for the patient's phenotype.

摘要

我们报告了一例新发的17q21.33微缺失,大小为1.8 Mb,在一名患有轻度智力障碍、生长发育迟缓、体重增加不佳、小头畸形、长脸、大喙鼻、下唇增厚、小颌畸形及其他畸形特征的患者中被检测到。该缺失通过全基因组基因分型BeadChip检测法检测到,涉及17号染色体上45,682,246至47,544,816 bp之间的基因组区域。该缺失所包含的24个RefSeq基因中,有参与脑发育和神经过程的CA10和CACNA1G基因。产前和产后生长发育迟缓的一个可能候选基因是CHAD基因,其产物软骨粘连蛋白是一种具有细胞结合特性的软骨蛋白。这三个基因可能是导致该患者表型的原因。

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