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- Material Type
- 文書・図像類
- Author/Editor
- 武田, 泰生
- Author Heading
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- Alternative Title
- Analysis of AICD in neurogenesis
- Text Language Code
- jpn
- Subject Heading
- Target Audience
- 一般
- Note (General)
- 2011-2013年度科学研究費助成事業（基盤研究（C））研究成果報告書 課題番号：23590190 研究代表者：武田泰生（鹿児島大学・医学部・歯学部附属病院・教授）アルツハイマー病の原因遺伝子として知られているアミロイド前駆蛋白質（APP）の細胞内領域（AICD）59アミノ酸残基をクローニングし、AICD強制発現系を構築した。このAICDプラスミドを一過性に導入したマウス胚性腫細胞P19細胞株において、レチノイン酸誘導化におけるAICD領域の神経分化への影響を、神経分化マーカーとして知られているTuj1ならびにMAP2遺伝子の発現量の差を定量PCR法により検討したところ、AICD導入細胞においてTuj1, MAP2が減少することを明らかにし、その途中過程において、幹細胞マーカーであるOct4の発現上昇による可能性を示唆した。Alzheimer's disease(AD)is a neurodegenerative disease and the most common form of dementia. Amyloid precursor protein(APP)plays a central role in the pathogenesis of AD. APP is type I transmembrane protein with a large extracellular domain and a short cytoplasmic domain(AICD59, AICD). AICD negatively modulates neurogenesis in neural precursor cells. However, the molecular mechanism of AICD have not been identified yet. In this study, we investigated the role of AICD in neuronal cell differentiation of P19 embryonic carcinoma cells. We have shown that P19 cells with induction Retinoic acid(RA) and transient overexpression of AICD could inhibit neural differentiation using qunantitative RT-PCR. Oct4, pluripotency stem cell marker was upregulated during the RA aggregated stage of AICD overexpressing P19 cells.Our data suggest that AICD may be involved in inhibited effect of neural differentiation during developmental brain.