SOD-1 inhibits FAS expression in cortex of APP transgenic mice.
SOD-1 inhibits FAS expression in cortex of APP transgenic mice.
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DOI：
10.1007/s10495-005-1879-y
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发表时间：
2005-05-01
期刊：
影响因子：
7.2
通讯作者：
Zhu, J
中科院分区：
文献类型：
--
作者：
Chen, Z;Duan, RS;Zhu, J
淀粉样前体蛋白 (APP) 的蛋白水解加工衍生的肽对于阿尔茨海默病 (AD) 的发病机制很重要。在本研究中，我们发现过表达野生型人类APP基因（hAPP/+）的转基因小鼠表现出更高的FAS（死亡受体亚家族之一）的表达。在过表达野生型 hAPP 基因和野生型人超氧化物歧化酶 1 基因 (hSOD-1) 的小鼠皮层中，这种 FAS 过表达显着降低。此外，hSOD-1 转基因表达与胶质纤维酸性蛋白 (GFAP) 产量的增加相关。这项研究表明 SOD-1 过度表达可以抑制 FAS 表达，这可能对 AD 有益。
Peptides derived from proteolytic processing of the amyloid precursor protein (APP) are important for the pathogenesis of Alzheimer's disease (AD). In the present study, we found that transgenic mice overexpressing wild-type human APP gene (hAPP/+) displayed a much higher expression of FAS, one of the death receptor subfamily. This FAS overexpression was significantly reduced in the cortex of mice overexpressing both wild-type hAPP gene and wild-type human superoxide dismutase-1 gene (hSOD-1). Moreover hSOD-1 transgenic expression was associated with an increase of Glial fibrillary acidic protein (GFAP) production. This study indicates that SOD-1 overexpression can inhibit FAS expression, which may be beneficial in AD.