Regulation of apoptosis by presenilin 1

被引：52

作者：

Wolozin, B ^{[1
]}

Alexander, P ^{[1
]}

Palacino, J ^{[1
]}

机构：

[1] Loyola Univ, Med Ctr, Dept Pharmacol, Maywood, IL 60153 USA

来源：

NEUROBIOLOGY OF AGING | 1998年 / 19卷 / 01期

关键词：

Alzheimer's disease; beta-amyloid; Fas; Jun Kinase; phosphorylation; neurodegeneration;

D O I：

10.1016/S0197-4580(98)00041-4

中图分类号：

R592 [老年病学]; C [社会科学总论];

学科分类号：

03 ; 0303 ; 100203 ;

摘要：

Familial Alzheimer's disease is transmitted as an autosomal dominant disorder and, in 5-10% of the cases, is caused by mutations in the coding regions of two homologous genes, Presenilin I and 2 (PS I and PS2). Previously, we have shown that PS2, a homolog of PS1, regulates apoptosis induced in neurons by trophic withdrawal or A beta, and in T-cells by Fas ligand. We now report that PS1 also regulates apoptosis. Both wild-type and the H115Y mutant form of PS1 enhance Pas-mediated apoptosis in Jurkat cells. We also observed that wild-type and the H115Y mutant form of PS1 differentially regulate Jun Kinase, an important enzyme regulating apoptosis. (C) 1998 Elsevier Science Inc.

引用

页码：S23 / S27

页数：5

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