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通过体外剪接试验确定已知 COL4A5 内含子变异的致病性。

Determination of the pathogenicity of known COL4A5 intronic variants by in vitro splicing assay.

机构信息

Department of Pediatrics, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo, Kobe, Hyogo, 650-0017, Japan.

Department of Child Health and Welfare (Pediatrics), Graduate School of Medicine, University of the Ryukyus, 207, Uehara, Nishihara-cho, Tyutou, Okinawa, 903-0125, Japan.

出版信息

Sci Rep. 2019 Sep 3;9(1):12696. doi: 10.1038/s41598-019-48990-9.

Abstract

X-linked Alport syndrome (XLAS) is a congenital renal disease caused by mutations in COL4A5. In XLAS cases suspected of being caused by aberrant splicing, transcript analysis needs to be conducted to determine splicing patterns and assess the pathogenicity. However, such analysis is not always available. We conducted a functional splicing assay using a hybrid minigene for seven COL4A5 intronic mutations: one was identified by us and six were found in the Human Gene Mutation Database. The minigene assay revealed exon skipping in four variants, exon skipping and a 10-bp insertion in one variant, and no change in one variant, which appeared not to be pathogenic. For one variant, our assay did not work. The results of all three cases for which transcript data were available were consistent with our assay results. Our findings may help to increase the accuracy of genetic test results and clarify the mechanisms causing aberrant splicing.

摘要

X 连锁遗传性肾炎(XLAS)是一种由 COL4A5 基因突变引起的先天性肾脏疾病。在疑似由异常剪接引起的 XLAS 病例中,需要进行转录本分析以确定剪接模式并评估其致病性。然而,并非总是能够进行这种分析。我们使用杂交小基因对 COL4A5 的七个内含子突变进行了功能剪接分析:一个是由我们鉴定的,六个是在人类基因突变数据库中发现的。小基因分析显示四个变体存在外显子跳跃,一个变体存在外显子跳跃和 10bp 插入,一个变体没有变化,似乎没有致病性。对于一个变体,我们的检测方法不起作用。对于所有三个可获得转录本数据的病例,结果与我们的检测结果一致。我们的发现可能有助于提高基因检测结果的准确性,并阐明导致异常剪接的机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88cb/6722096/8a54e91b8ffc/41598_2019_48990_Fig1_HTML.jpg

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