Alternative cleavage of Alzheimer-associated presenilins during apoptosis by a caspase-3 family protease

被引：327

作者：

Kim, TW

Pettingell, WH

Jung, YK

Kovacs, DM

Tanzi, RE

机构：

[1] HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,DEPT NEUROL,GENET & AGING UNIT,CHARLESTOWN,MA 02129

[2] KWANGJU INST SCI & TECHNOL,DEPT LIFE SCI,KWANGJU,SOUTH KOREA

来源：

SCIENCE | 1997年 / 277卷 / 5324期

关键词：

D O I：

10.1126/science.277.5324.373

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：

Most cases of early-onset familiar Alzheimer's disease (FAD) are caused by mutations in the genes encoding the presenilin 1 (PS1) and PS2 proteins, both of which undergo regulated endoproteolytic processing. During apoptosis, PS1 and PS2 were shown to be cleaved at sites distal to their normal cleavage sites by a caspase-3 family protease. In cells expressing PS2 containing the asparagine-141 FAD mutant, the ratio of alternative to normal PS2 cleavage fragments was increased relative to wild-type PS2-expressing cells, suggesting a potential role for apoptosis-associated cleavage of presenilins in the pathogenesis of Alzheimer's disease.

引用

页码：373 / 376

页数：4

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