Overexpression of a C-terminal fragment of Presenilin 1 delays anti-Fas induced apoptosis in Jurkat cells

被引：13

作者：

Vézina, J ^{[1
]}

Tschopp, C ^{[1
]}

Andersen, E ^{[1
]}

Müller, K ^{[1
]}

机构：

[1] Novartis Pharma Ltd, Preclin Res, CH-4002 Basel, Switzerland

来源：

NEUROSCIENCE LETTERS | 1999年 / 263卷 / 01期

关键词：

apoptosis; Alzheimer's disease; presenilin; 1; flow cytometry; green fluorescent peptide; tetracycline-off system; Jurkat cells;

D O I：

10.1016/S0304-3940(99)00097-X

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Most cases of early onset familial Alzheimer's disease (FAD) involve mutations in presenilins (PSI and PS2) genes. The C-terminal portion of PS2 is a homologue with an apoptosis-linked gene (ALG-3). To characterise the role of PSI in apoptosis, we overexpressed the corresponding C-terminal fragment of PSI (PS1-f) under the control of the tetracycline-responsive transactivator in Jurkat cells. The tight regulation of the expression of the 11 kDa PS1-f peptide was verified. A 50% inhibition of anti-fas induced apoptosis was observed upon PS1-f transient overexpression compared to the repressed state. Stable transfectants selectively overexpressing PS1-f revealed a transient protective effect of 30% after apoptosis induction. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.

引用

页码：65 / 68

页数：4

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