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靶向二代测序在印度患者中鉴定出ANK1基因导致严重遗传性球形红细胞增多症的新的有害变异:拓展分子和临床谱

Targeted next-generation sequencing identifies novel deleterious variants in ANK1 gene causing severe hereditary spherocytosis in Indian patients: expanding the molecular and clinical spectrum.

作者信息

More Tejashree Anil, Devendra Rati, Dongerdiye Rashmi, Warang Prashant, Kedar Prabhakar

机构信息

Department of Haematogenetics, ICMR-National Institute of Immunohematology, Indian Council of Medical Research, 13th Floor, New Multi-Storeyed Building, King Edward Memorial (KEM.) Hospital Campus, Parel, Mumbai, 400012, India.

出版信息

Mol Genet Genomics. 2023 Mar;298(2):427-439. doi: 10.1007/s00438-022-01984-1. Epub 2023 Jan 4.

Abstract

Hereditary Spherocytosis (HS) is a common cause of hemolytic anemia varying from mild to severe hemolysis due to defects in red cell membrane protein genes, namely ANK1, SPTB, SPTA1, SLC4A1, and EPB42. These genes are considerably very large spaning 40-50 exons making gene-by-gene analysis costly and laborious by conventional methods. In this study, we explored 26 HS patients harboring 21 ANK1 variants identified by next-generation sequencing (NGS), characteristics and spectrum of the detected ANK1variants were analyzed in this study. Clinically, all the HS patients showed moderate to severe transfusion-dependent hemolytic anemia, some requiring splenectomy. We identified 13 novel and 8 reported variants, mainly 9 frameshifts, 2 missense, 6 nonsense, and 4 splice site ANK1 variants, using NGS technology. Frameshifts were remarkably the most common variant type seen in Indian HS patients with ANK1 gene defects. We have also explored expression levels of red cell membrane ankyrin protein by flow cytometry in 14 HS patients with ANK1 gene defects and a significant reduction in ankyrin protein expression has been found. This report mainly illustrates the molecular and phenotypic heterogeneity of ANK1 variants causing HS in Indian patients. Ankyrin-1 mutations are a significant cause of loss of function in dominant HS in the Indian population. Comprehensive genetic and phenotypic evaluation assists in implementing the knowledge of genetic patterns and spectrum of ANK1 gene variants, providing molecular support for HS diagnosis.

摘要

遗传性球形红细胞增多症(HS)是溶血性贫血的常见病因,由于红细胞膜蛋白基因(即ANK1、SPTB、SPTA1、SLC4A1和EPB42)存在缺陷,溶血程度从轻度到重度不等。这些基因跨度相当大,有40 - 50个外显子,采用传统方法逐个基因分析成本高且费力。在本研究中,我们对26例通过下一代测序(NGS)鉴定出携带21种ANK1变异的HS患者进行了研究,分析了检测到的ANK1变异的特征和谱系。临床上,所有HS患者均表现为中度至重度输血依赖型溶血性贫血,部分患者需要进行脾切除术。我们使用NGS技术鉴定出13种新变异和8种已报道的变异,主要为9种移码变异、2种错义变异、6种无义变异和4种剪接位点ANK1变异。移码变异明显是印度ANK1基因缺陷型HS患者中最常见的变异类型。我们还通过流式细胞术检测了14例ANK1基因缺陷型HS患者红细胞膜锚蛋白的表达水平,发现锚蛋白表达显著降低。本报告主要阐述了印度患者中导致HS的ANK1变异的分子和表型异质性。锚蛋白-1突变是印度人群显性HS功能丧失的重要原因。全面的基因和表型评估有助于了解ANK1基因变异的遗传模式和谱系,为HS诊断提供分子支持。

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