Binini N, Sancini G, Villa C, Dal Magro R, Sansoni V, Rusconi R, Mantegazza M, Grioni D, Talpo F, Toselli M, Combi R
Department of Biology and Biotechnology "L. Spallanzani", University of Pavia, 27100 Pavia, Italy.
School of Medicine and Surgery, University of Milano-Bicocca, Monza, Italy; Neuroscience Center of University of Milano Bicocca Monza, Italy.
Brain Res. 2017 Dec 15;1677:26-32. doi: 10.1016/j.brainres.2017.09.023. Epub 2017 Sep 23.
Mutations in the SCN1A gene causing either loss or gain of function have been frequently found in patients affected by genetic epilepsy with febrile seizures plus (GEFS+) or Dravet syndrome (also named severe myoclonic epilepsy in infancy SMEI). By mutation screening of the SCN1A gene, we identified for the first time a case of two missense mutations in cis (p.[Arg1525Gln;Thr297Ile]) in all affected individuals of an Italian family showing GEFS+ and idiopathic generalized epilepsy (IGE). The p.Arg1525Gln mutation was not previously reported yet and was predicted to be pathological by prediction tools, whereas the p.Thr297Ile was already identified in patients showing SMEI. Functional studies revealed that the Nav1.1 channels harboring both mutations were characterized by a significant shift in the activation curve towards more positive potentials. Our data demonstrate that the p.Arg1525Gln represents a novel mutation in the SCN1A gene altering the channel properties in the co-presence of the p.Thr297Ile.
在患有热性惊厥附加症(GEFS+)或Dravet综合征(也称为婴儿严重肌阵挛性癫痫,SMEI)的患者中,经常发现SCN1A基因发生功能丧失或功能获得性突变。通过对SCN1A基因进行突变筛查,我们首次在一个表现为GEFS+和特发性全身性癫痫(IGE)的意大利家族的所有患病个体中,鉴定出一例顺式存在的两个错义突变(p.[Arg1525Gln;Thr297Ile])。p.Arg1525Gln突变此前尚未见报道,预测工具预测其为病理性突变,而p.Thr297Ile已在表现为SMEI的患者中被鉴定出。功能研究表明,携带这两种突变的Nav1.1通道的特征是激活曲线向更正电位显著偏移。我们的数据表明,p.Arg1525Gln代表SCN1A基因中的一种新突变,在p.Thr297Ile共存的情况下改变了通道特性。