JAG1
错义突变
移码突变
阿拉吉尔综合征
单倍率不足
遗传学
生物
无义突变
突变
外显子
基因
基因突变
表型
分子生物学
Notch信号通路
胆汁淤积
内分泌学
作者
Giuseppe Pilia,Manuela Uda,Dolores Macis,Fulvia Frau,Laura Crisponi,Fiorella Balli,Cristiana Barbera,Carla Colombo,T. Frediani,Rosanna Gatti,Raffaele Iorio,Maria Grazia Marazzi,Matilde Marcellini,S Musumeci,Gabriella Nebbia,Pietro Vajro,G Ruffa,Lucia Zancan,Antonio Cao,S. DeVirgilis
标识
DOI:10.1002/(sici)1098-1004(199911)14:5<394::aid-humu5>3.0.co;2-1
摘要
Alagille syndrome (AGS) is an autosomal dominant disorder with developmental abnormalities affecting the liver, heart, eyes, vertebrae, and craniofacial region. The Jagged-1 (JAG1) gene, which encodes a ligand of Notch, has recently been found mutated in AGS. In this study, mutation analysis of the JAG1 gene performed on 20 Italian AGS patients led to the identification of 15 different JAG1 mutations, including a large deletion of the 20p12 region, six frameshift, three nonsense, three splice-site, and two missense mutations. The two novel missense mutations were clustered in the 5' region, while the remaining mutations were scattered throughout the gene. The spectrum of mutations in Italian patients was similar to that previously reported. We also studied in detail a complex splice site mutation, 3332dupl8bp, which was shown to lead to an abnormal JAG1 mRNA, resulting in a premature stop codon. With the exception of the missense mutations, the majority of the JAG1 mutations are therefore likely to produce truncated proteins. Since the phenotype of the patient with a complete deletion of the JAG1 gene is indistinguishable from that of patients with intragenic mutations, our study further supports the hypothesis that haploinsufficiency is the most common mechanism involved in AGS pathogenesis. Furthermore, our data confirmed the absence of a correlation between the genotype of the JAG1 gene and the AGS phenotype.
科研通智能强力驱动
Strongly Powered by AbleSci AI