Mayatepek E, Nezu J, Tamai I, Oku A, Katsura M, Shimane M, Tsuji A
Department of General Pediatrics, University Children's Hospital, Heidelberg, Germany.
Hum Mutat. 2000 Jan;15(1):118. doi: 10.1002/(SICI)1098-1004(200001)15:1<118::AID-HUMU28>3.0.CO;2-8.
Primary systemic carnitine deficiency (SCD) is an autosomal recessive disorder of fatty acid oxidation caused by defective cellular carnitine transport. The disease is characterized by metabolic derangement simulating Reye's syndrome, hypoglcaemia, progressive cardiomyopathy and skeletal myopathy. Recently, it was shown that SCD is caused by mutations in the organic cation/carnitine transporter OCTN2 (SLC22A5). We report two novel mutations, W283R and V446F, which are both missense mutations in an affected infant. In vitro expression studies demonstrated that both are actually function-loss mutations with virtually no uptake activity. This is the first report of compound heterozygosity for two missense mutations in a patient with SCD. Hum Mutat 15:118, 2000.
原发性系统性肉碱缺乏症(SCD)是一种常染色体隐性脂肪酸氧化障碍疾病,由细胞肉碱转运缺陷引起。该疾病的特征为代谢紊乱,类似瑞氏综合征、低血糖、进行性心肌病和骨骼肌病。最近研究表明,SCD是由有机阳离子/肉碱转运体OCTN2(SLC22A5)的突变所导致。我们报告了两个新的突变,W283R和V446F,这两个都是一名患病婴儿中的错义突变。体外表达研究表明,这两个突变实际上都是功能丧失性突变,几乎没有摄取活性。这是关于SCD患者中两个错义突变的复合杂合性的首次报道。《人类突变》15:118,2000年。