Direct association of presenilin-1 with β-catenin
Direct association of presenilin-1 with β-catenin
复制标题
DOI：
10.1016/s0014-5793(98)00886-2
复制
发表时间：
1998-08-14
期刊：
影响因子：
3.5
通讯作者：
Takashima, A
中科院分区：
文献类型：
--
作者：
Murayama, M;Tanaka, S;Takashima, A
早老素-1（PS1）基因突变的家族可导致阿尔茨海默病（AD），但PS1导致AD的机制尚不清楚。在转染的COS-7细胞中与PS 1的免疫共沉淀表明PS 1直接与内源性β-catenin相互作用，并且这种相互作用需要PS 1的322-450位残基和β-catenin的445-676位残基，这两种蛋白质共定位于内质网，PS 1的过表达降低了胞浆β-catenin的水平，并抑制了β-catenin-T细胞因子调节的转录，这些结果表明，PS1作为β-连环蛋白信号的抑制剂发挥作用，这可能与AD功能障碍有关，（C）1998年欧洲生物化学学会联合会。
Families bearing mutations in the presenilin-1 (PS1) gene develop Alzheimer's disease (AD), However, the mechanism through which PS1 causes AD is unclear. The co-immunoprecipitation with PS1 in transfected COS-7 cells indicates that PS1 directly interacts with endogenous beta-catenin, and the interaction requires residues 322-450 of PS1 and 445-676 of beta-catenin, Both proteins are co-localized in the endoplasmic reticulum, Over-expression of PS1 reduces the level of cytoplasmic beta-catenin, and inhibits beta-catenin-T cell factor-regulated transcription, These results indicate that PS1 plays a role as inhibitor of the beta-catenin signal, which may be connected with the AD dysfunction, (C) 1998 Federation of European Biochemical Societies.