Requirement of the familial Alzheimer's disease gene PS2 for apoptosis - Opposing effect of ALG-3
Requirement of the familial Alzheimer's disease gene PS2 for apoptosis - Opposing effect of ALG-3
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DOI：
10.1074/jbc.271.49.31025
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发表时间：
1996-12-06
影响因子：
4.8
通讯作者：
DAdamio, L
中科院分区：
文献类型：
--
作者：
Vito, P;Wolozin, B;DAdamio, L
ALG-3是家族性阿尔茨海默病基因PS2的截短的小鼠同源基因，通过抑制Fas配体诱导和Fas信号转导来拯救T杂交瘤3DO细胞免于T细胞受体诱导的细胞凋亡。在这里，我们表明ALG-3转染的3DO细胞表达COOH末端的PS2多肽。在ALG-3转染的3DO细胞中PS2的过表达重建了对受体诱导的细胞死亡的敏感性，提示人工PS2多肽作为PS2的显性负突变体发挥作用，ALG-3和反义PS2保护PC 12细胞免于谷氨酸诱导的凋亡，但不保护由过氧化氢或自由基MPP（+）诱导的死亡。因此，PS2基因是不同细胞类型中某些形式的细胞死亡所必需的，并且其功能与ALG-3相反。
ALG-3, a truncated mouse homologue of the chromosome I familial Alzheimer's disease gene PS2, rescues T hybridoma 3DO cells from T-cell receptor-induced apoptosis by inhibiting Fas ligand induction and Fas signaling, Here we show that ALG-3 transfected 3DO cells express a COOH-terminal PS2 polypeptide, Overexpression of PS2 in ALG-3 transfected 3DO cells reconstitutes sensitivity to receptor-induced cell death, suggesting that the artificial PS2 polypeptide functions as a dominant negative mutant of PS2, ALG-3 and antisense PS2 protect PC12 cells from glutamate-induced apoptosis but not from death induced by hydrogen peroxide or the free radical MPP(+). Thus, the PS2 gene is required for some forms of cell death in diverse cell types, and its function is opposed by ALG-3.