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由 TLK2 纯合变体引起的严重神经发育疾病。

Severe neurodevelopmental disease caused by a homozygous TLK2 variant.

机构信息

John Walton Muscular Dystrophy Research Centre, Institute of Genetic Medicine, Newcastle University, Newcastle upon Tyne, UK.

Izmir Biomedicine and Genome Center, Dokuz Eylul University Health Campus, Izmir, Turkey.

出版信息

Eur J Hum Genet. 2020 Mar;28(3):383-387. doi: 10.1038/s41431-019-0519-x.

Abstract

A distinct neurodevelopmental phenotype characterised mainly by mild motor and language delay and facial dysmorphism, caused by heterozygous de novo or dominant variants in the TLK2 gene has recently been described. All cases reported carried either truncating variants located throughout the gene, or missense changes principally located at the C-terminal end of the protein mostly resulting in haploinsufficiency of TLK2. Through whole exome sequencing, we identified a homozygous missense variant in TLK2 in a patient showing more severe symptoms than those previously described, including cerebellar vermis hypoplasia and West syndrome. Both parents are heterozygous for the variant and clinically unaffected highlighting that recessive variants in TLK2 can also be disease causing and may act through a different pathomechanism.

摘要

最近描述了一种明显的神经发育表型,主要表现为轻度运动和语言延迟以及面部畸形,由 TLK2 基因的杂合性新生或显性变异引起。所有报道的病例均携带整个基因中的截断变异,或主要位于蛋白质 C 末端的错义变化,主要导致 TLK2 的单倍不足。通过全外显子组测序,我们在一名表现出比以前描述的更严重症状的患者中发现了 TLK2 中的纯合错义变异,包括小脑蚓部发育不良和 West 综合征。父母双方均为该变异的杂合子且临床不受影响,这突出表明 TLK2 中的隐性变异也可能是致病的,并且可能通过不同的病理机制起作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e6b/7028915/11fcbccc5377/41431_2019_519_Fig1_HTML.jpg

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