MUTATION OF GLU693 TO GLN OR VAL717 TO ILE HAS NO EFFECT ON THE PROCESSING OF ALZHEIMER AMYLOID PRECURSOR PROTEIN EXPRESSED IN COS-1 CELLS BY CDNA TRANSFECTION

被引：26

作者：

MARUYAMA, K ^{[1
]}

USAMI, M ^{[1
]}

YAMAOHARIGAYA, W ^{[1
]}

TAGAWA, K ^{[1
]}

ISHIURA, S ^{[1
]}

机构：

[1] NATL INST NEUROSCI,KODAIRA,TOKYO,JAPAN

来源：

NEUROSCIENCE LETTERS | 1991年 / 132卷 / 01期

关键词：

ALZHEIMERS DISEASE; AMYLOID PRECURSOR PROTEIN; AMYLOID BETA-PROTEIN; COS-1; CELL; SECRETASE; PROCESSING; MUTATION;

D O I：

10.1016/0304-3940(91)90442-V

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

One of the features of Alzheimer's disease (AD) is the formation of senile plaques, of which the main component is a 42 amino acid beta-protein (beta-P). Molecular cloning of beta-P revealed the presence of a 90-130 kDa precursor, amyloid precursor protein (APP). Since APP is expressed in normal brain without producing beta-P, some abnormal processing is the cause of the formation of beta-P in AD. Two kinds of mutations of APP, Glu693 to Gln and Val717 to Ile, were reported in AD-related diseases. Site-directed mutagenesis was applied, and the mutated APPs were expressed in COS-1 cells by cDNA transfection. They showed apparently the same processing as wild APP. This means that these mutations might not be a direct cause for the abnormal processing of APP or the formation of beta-P in AD.

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页码：97 / 100

页数：4

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