Estivill X, Lázaro C, Casals T, Ravella A
Molecular Genetics Department, Hospital Duran y Reynals, Barcelona, Spain.
Hum Genet. 1991 Dec;88(2):185-8. doi: 10.1007/BF00206069.
The gene responsible for von Recklinghausen neurofibromatosis (NF1) has recently been identified, and several point mutations and deletions have been described. The availability of intron-exon boundaries of several exons of the NF1 gene facilitates the search for mutations in affected patients. We have analysed 38 patients for mutations in exon 4 of the NF1 gene, and found one patient with a C----T transition at base position 1087 of the cDNA, changing an arginine codon to a stop codon, at amino acid position 365. Sequencing of other members of the family, including both parents, did not show the mutation, confirming that this mutation is responsible for this sporadic NF1 case. As the mutation described here was previously identified in an independent case by others, this case represents a recurrence of this mutation and suggests that codon 365 might be a hot spot for mutations in the NF1 gene. Thus, a specific search for this mutation should be performed when studying NF1 sporadic or familiar cases for genetic analysis.
导致冯·雷克林霍增氏神经纤维瘤病(NF1)的基因最近已被确定,并且已描述了几种点突变和缺失情况。NF1基因几个外显子的内含子 - 外显子边界信息有助于在受影响患者中寻找突变。我们分析了38例患者的NF1基因第4外显子中的突变,发现1例患者在cDNA的第1087个碱基位置发生了C→T转换,将精氨酸密码子变为终止密码子,位于氨基酸位置365。对该家族其他成员(包括父母)的测序未显示该突变,证实此突变是导致该散发性NF1病例的原因。由于此处描述的突变先前已被其他人在一个独立病例中鉴定出来,该病例代表了此突变的再次出现,并表明密码子365可能是NF1基因中的一个突变热点。因此,在研究NF1散发性或家族性病例进行遗传分析时,应针对此突变进行特定的检测。