肌萎缩侧索硬化转基因模型脊髓中亲免素FKBP 52的早期减少。
Early decrease of the immunophilin FKBP 52 in the spinal cord of a transgenic model for amyotrophic lateral sclerosis.
作者信息
Manabe Y, Warita H, Murakami T, Shiote M, Hayashi T, Omori N, Nagano I, Shoji M, Abe K
机构信息
Department of Neurology, Graduate School of Medicine and Dentistry, Okayama University, 2-5-1 Shikata-cho, Okayama 700-8558, Japan.
出版信息
Brain Res. 2002 May 10;935(1-2):124-8. doi: 10.1016/s0006-8993(02)02466-6.
Expressions of immunophilin FKBP-12 and FKBP-52 were examined in the spinal cord of transgenic mice with an ALS-linked mutant Cu/Zn superoxide dismutase (SOD1) gene. The immunoreactivity of FKBP-12 was present predominantly in the cytoplasm, but did not show a difference between age-matched wild type and transgenic (Tg) mice at 25 and 35 weeks. In contrast, the immunoreactivity of FKBP-52 was predominantly present in the nucleus, which progressively declined only in the Tg mice as early as an early presymptomatic stage at 25 weeks of age in the anterior horn neurons. The present result suggests that the downregulation of FKBP-52 may be involved in the pathogenesis in the early stages of amyotrophic lateral sclerosis (ALS).
在携带与肌萎缩侧索硬化症（ALS）相关的突变型铜锌超氧化物歧化酶（SOD1）基因的转基因小鼠脊髓中检测了免疫亲和蛋白FKBP - 12和FKBP - 52的表达。FKBP - 12的免疫反应性主要存在于细胞质中，但在25周和35周时，年龄匹配的野生型和转基因（Tg）小鼠之间未显示出差异。相比之下，FKBP - 52的免疫反应性主要存在于细胞核中，早在25周龄前症状期的前角神经元中，仅在Tg小鼠中其免疫反应性逐渐下降。目前的结果表明，FKBP - 52的下调可能参与了肌萎缩侧索硬化症（ALS）早期的发病机制。
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