APOLIPOPROTEIN-E UPTAKE AND DEGRADATION VIA CHLOROQUINE-SENSITIVE PATHWAY IN CULTIVATED MONKEY CELLS OVEREXPRESSING LOW-DENSITY-LIPOPROTEIN RECEPTOR

被引：13

作者：

JENSEN, TG

ROSES, AD

JORGENSEN, AL

机构：

[1] AARHUS UNIV,INST HUMAN GENET,DK-8000 AARHUS C,DENMARK

[2] DUKE UNIV,MED CTR,JOSEPH & KATHLEEN BRYAN ALZHEIMERS DIS RES CTR,DEPT MED & NEUROSCI,DURHAM,NC

来源：

NEUROSCIENCE LETTERS | 1994年 / 180卷 / 02期

关键词：

ALZHEIMERS DISEASE; PATHOGENESIS; MODEL SYSTEMS; COS CELL; LIPOFECTION; CEREBROSPINAL FLUID; IMMUNOSTAINING;

D O I：

10.1016/0304-3940(94)90519-3

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Alzheimer's disease with late onset is associated with inheritance of isoform 4 of the polymorphic apolipoprotein E (ApoE). We describe an experimental model where intracellular interaction between ApoE isoforms and cellular proteins may be studied. Internalization and intracellular fate of ApoE from fresh normal cerebrospinal fluid is followed in COS cells (an SV40 transformed Simian kidney cell line) overexpressing the low density lipoprotein receptor. Chase and chloroquine experiments strongly suggest that internalized ApoE travels through the endosomal-lysosomal pathway after dissociation from the receptor in early endosome.

引用

页码：193 / 196

页数：4

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