Differential regulation of APP secretion by apolipoprotein E3 and E4

被引：12

作者：

Wolozin, BL ^{[1
]}

BasaricKeys, J ^{[1
]}

Canter, R ^{[1
]}

Li, Y ^{[1
]}

Vanderputten, D ^{[1
]}

Sunderland, T ^{[1
]}

机构：

[1] NIMH,LAB BIOCHEM GENET,BETHESDA,MD 20892

来源：

NEUROBIOLOGY OF ALZHEIMER'S DISEASE | 1996年 / 777卷

关键词：

D O I：

10.1111/j.1749-6632.1996.tb34440.x

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

The apolipoprotein E isozyme, apolipoprotein E4, has been implicated as a risk factor for Alzheimer's disease. One reason for the increased risk may be that apolipoprotein E binds to the AP peptide, but there may be other factors as well. We show that apolipoprotein E is a potent regulator of the secretion of amyloid precursor protein. In cultures of PC12 cells, nanomolar levels of apolipoprotein E3 induce a rapid decrease in the secretion of APP, being observable in 30 min. and stable over 24 hours. Apolipoprotein E4, in contrast, increases secretion of APP over a similar time course. Reciprocal changes occur in cellular amyloid precursor protein. Differential characteristics are also seen in apo E binding to the cells, where apo E4 binds over a slower time course than apo E3. These results suggest a novel mechanism by which apolipoprotein E may be influencing the metabolism of amyloid precursor protein.

引用

页码：322 / 326

页数：5

共 7 条

[1] GENE DOSE OF APOLIPOPROTEIN-E TYPE-4 ALLELE AND THE RISK OF ALZHEIMERS-DISEASE IN LATE-ONSET FAMILIES [J].