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马凡综合征家族病例中的FBN1基因内含子深部突变:能否解释基因未明确的病例?

An FBN1 deep intronic mutation in a familial case of Marfan syndrome: an explanation for genetically unsolved cases?

作者信息

Gillis Elisabeth, Kempers Marlies, Salemink Simone, Timmermans Janneke, Cheriex Emile C, Bekkers Sebastiaan C A M, Fransen Erik, De Die-Smulders Christine E M, Loeys Bart L, Van Laer Lut

机构信息

Center for Medical Genetics, Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium.

出版信息

Hum Mutat. 2014 May;35(5):571-4. doi: 10.1002/humu.22540. Epub 2014 Apr 7.

Abstract

Marfan syndrome (MFS) is caused by mutations in the FBN1 (fibrillin-1) gene, but approximately 10% of MFS cases remain genetically unsolved. Here, we report a new FBN1 mutation in an MFS family that had remained negative after extensive molecular genomic DNA FBN1 testing, including denaturing high-performance liquid chromatography, Sanger sequencing, and multiplex ligation-dependent probe amplification. Linkage analysis in the family and cDNA sequencing of the proband revealed a deep intronic point mutation in intron 56 generating a new splice donor site. This mutation results in the integration of a 90-bp pseudo-exon between exons 56 and 57 containing a stop codon, causing nonsense-mediated mRNA decay. Although more than 90% of FBN1 mutations can be identified with regular molecular testing at the genomic level, deep intronic mutations will be missed and require cDNA sequencing or whole-genome sequencing.

摘要

马凡综合征(MFS)由FBN1(原纤蛋白-1)基因突变引起,但约10%的MFS病例在基因层面仍未得到明确诊断。在此,我们报告了一个MFS家族中的新型FBN1突变,在进行包括变性高效液相色谱、桑格测序和多重连接依赖探针扩增在内的广泛分子基因组DNA FBN1检测后,该家族检测结果仍为阴性。对该家族进行连锁分析以及对先证者进行cDNA测序,发现内含子56存在一个深度内含子点突变,产生了一个新的剪接供体位点。此突变导致外显子56和57之间整合了一个包含终止密码子的90 bp假外显子,引发无义介导的mRNA降解。尽管通过常规的基因组水平分子检测可以识别超过90%的FBN1突变,但深度内含子突变会被遗漏,需要进行cDNA测序或全基因组测序。

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