SAMHD1公司
突变
复合杂合度
综合征如奈梅亨破损综合症
医学
遗传学
外显子组测序
发病机制
表型
阿达尔
基因
生物
病理
基因表达
DNA损伤
DNA
聚合酶链反应
逆转录酶
共济失调毛细血管扩张
RNA编辑
作者
Barbara Oleksy,Hanna Mierzewska,Jolanta Tryfon,Maria Wypchło,Krystyna Wasilewska,Zofia Zalewska‐Miszkurka,Rafał Płoski,Małgorzata Rydzanicz,Elżbieta Szczepanik
摘要
We report on the first Polish patient diagnosed with the Aicardi-Goutières syndrome 5 (AGS5). AGS is caused by mutations in one of 9 genes (TREX1, RNASEH2A, RNASEH2B, RNASEH2C, SAMHD1, ADAR, IFIH, LSM11, RNU7-1) which stimulate the type I interferon response. The diagnosis was confirmed by identifying a compound heterozygous mutation p.(Phe165Ser)/p.(Gln235*) in the SAMHD1 gene using whole-exome sequencing. The cystic lesions in the temporal lobes are an uncommon finding in the presented patient carrying a SAMHD1 mutation. Reporting new cases expands the range of phenotypes and plays the crucial role in understanding the AGS pathogenesis and creates new therapy approaches.
科研通智能强力驱动
Strongly Powered by AbleSci AI