Brooks A S, Dooijes D
Erasmus Medisch Centrum, afd. Klinische Genetica, Dr. Molewaterplein 50, 3015 GE Rotterdam.
Ned Tijdschr Geneeskd. 2003 Jun 21;147(25):1213-5.
Alagille syndrome (AGS), also known as arteriohepatic dysplasia, is an autosomal dominant disorder with a prevalence of approximately one in 70,000 live births. AGS is characterised by intrahepatic bile duct paucity and other developmental abnormalities affecting the heart, liver, eyes, vertebrae and the craniofacial region. Mutations in the JAG1 gene have been demonstrated to cause Alagille syndrome. JAG1 encodes a cellular membrane-bound ligand for the Notch receptor and is expressed during the normal development of tissues affected in Alagille syndrome. JAG1 mutations are detected in approximately 70% of AGS patients and are mostly protein truncating mutations. JAG1 mutations have also been described in patients that do not demonstrate the complete AGS phenotype, suggesting that the phenotypic spectrum of JAG1 mutations is broader than thus far assumed.
阿拉吉耶综合征(AGS),也称为动脉肝发育不良,是一种常染色体显性疾病,在活产婴儿中的患病率约为7万分之一。AGS的特征是肝内胆管稀少以及影响心脏、肝脏、眼睛、脊椎和颅面部区域的其他发育异常。已证明JAG1基因突变会导致阿拉吉耶综合征。JAG1编码Notch受体的一种细胞膜结合配体,并在阿拉吉耶综合征所影响组织的正常发育过程中表达。约70%的AGS患者检测到JAG1突变,且大多为蛋白质截短突变。在未表现出完整AGS表型的患者中也描述了JAG1突变,这表明JAG1突变的表型谱比迄今所认为的更广泛。