移码突变
严重联合免疫缺陷
外显子组测序
腺苷脱氨酶缺乏症
免疫缺陷
突变
基因
生物
遗传学
腺苷脱氨酶
基因检测
免疫系统
生物化学
腺苷
作者
Taravat Talebi,Alirezai Biglari,Mohammad Shahroeei,Majid Changi‐Ashtiani,Hossein Dinmohammadi,Shadi Sadat Navabi,Nima Parvaneh,Xavier Bossuyt,Tina Shahani,Hassan Rokni‐Zadeh
标识
DOI:10.18502/ijaai.v19i1.2422
摘要
Severe combined immunodeficiency (SCID) comprises a heterogeneous group of genetic disorders caused by early defects in the development and function of T cells. Other lymphocyte lineages (B and/or natural killer cells) are variably affected. With a worldwide frequency of approximately 1:50,000 live births, SCID may result from diverse mutations in over 16 genes. Whole-exome sequencing (WES) provides an opportunity for parallel screening of all those genes. This approach is also useful for genetic diagnosis in parents whose infant expired before genetic testing. Here, we describe a heterozygous novel non-frameshift deletion (c.587_598del p.196_199del) in the adenosine deaminase (ADA) gene identified by WES in healthy parents of an expired child with SCID. The mutation was subsequently confirmed to be homozygous in the deceased baby whose left-over blood sample volume was insufficient for direct WES analysis. In conclusion, we here describe a novel mutation in ADA, a well-known SCID gene.
科研通智能强力驱动
Strongly Powered by AbleSci AI