Jilin Medical University, Jilin, China.
National Engineering Laboratory for AIDS Vaccine, School of Life Sciences, Jilin University, Changchun, China.
J Dermatol. 2018 Aug;45(8):986-988. doi: 10.1111/1346-8138.14493. Epub 2018 Jun 28.
Neurofibromatosis type 1 (NF1), caused by germ line mutations of the NF1 tumor-suppressor gene, is one of the most common autosomal dominant disorders. Here, we reported a NF1 patient with the mutation NF1 c.4367+1G>C. This sequence change locates at the first nucleotide of NF1 intron 32 within the consensus splice site. Compared with NF1 c.4367G>C predicted to potentially damage the wild-type donor site at c.4367, the NF1 c.4367+1G>C potentially abolishes this wild-type donor site by in silico analysis. In vitro minigene assay revealed that the NF1 c.4367+1G>C may cause exon 32 skipping. Our result provides further evidence for its clinical significance of NF1 c.4367+1G>C in clinical practise.
神经纤维瘤病 1 型(NF1)是由 NF1 肿瘤抑制基因的种系突变引起的,是最常见的常染色体显性遗传疾病之一。在这里,我们报告了一例 NF1 患者,其突变 NF1 c.4367+1G>C。该序列变化位于 NF1 内含子 32 内的一致剪接位点的第一个核苷酸处。与预测可能破坏 c.4367 处野生型供体位点的 NF1 c.4367G>C 相比,NF1 c.4367+1G>C 通过计算机分析可能使该野生型供体位点失活。体外小基因试验表明,NF1 c.4367+1G>C 可能导致外显子 32 跳跃。我们的结果为 NF1 c.4367+1G>C 在临床实践中的临床意义提供了进一步的证据。