NPC1
尼曼-皮克病
生物
胆固醇
肝X受体
互补DNA
错义突变
基因
化学
细胞生物学
生物化学
内体
细胞内
突变
转录因子
核受体
作者
Eugene D. Carstea,Jill A. Morris,Katherine Coleman,Stacie K. Loftus,Dana Zhang,Christiano Cummings,Jessie Gu,Melissa A. Rosenfeld,William J. Pavan,David B. Krizman,James W. Nagle,Mihail H. Polymeropoulos,Stephen L. Sturley,Yiannis A. Ioannou,Maureen E. Higgins,Marcella Comly,Adele Cooney,Anthony Brown,Christine R. Kaneski,E. Joan Blanchette‐Mackie
出处
期刊:Science
[American Association for the Advancement of Science]
日期:1997-07-11
卷期号:277 (5323): 228-231
被引量:1462
标识
DOI:10.1126/science.277.5323.228
摘要
Niemann-Pick type C (NP-C) disease, a fatal neurovisceral disorder, is characterized by lysosomal accumulation of low density lipoprotein (LDL)-derived cholesterol. By positional cloning methods, a gene (NPC1) with insertion, deletion, and missense mutations has been identified in NP-C patients. Transfection of NP-C fibroblasts with wild-type NPC1 cDNA resulted in correction of their excessive lysosomal storage of LDL cholesterol, thereby defining the critical role of NPC1 in regulation of intracellular cholesterol trafficking. The 1278-amino acid NPC1 protein has sequence similarity to the morphogen receptor PATCHED and the putative sterol-sensing regions of SREBP cleavage-activating protein (SCAP) and 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase.
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