プロトオンコゲンbcl-2は,アポプトーシスによる神経縮因子依存ニューロンを選択的に救出することができます
T E Allsopp1, S Wyatt, H F Paterson
1School of Biological and Medical Sciences, St. Andrews, Fife, Scotland.
Cell
|April 23, 1993
まとめ
bcl-2遺伝子製品は,一部のニューロンにおけるアポトーシスを防ぐことができますが,すべてではありません. 特定の神経栄養素因子の影響を受け,異なる神経死経路が存在する.
科学分野:
- 神経科学は神経科学である.
- 分子生物学は分子生物学である.
- 細胞生物学 細胞生物学
背景:
- アポトーシスは,発達中の細胞数を調節するために不可欠です.
- bcl-2遺伝子製品は,骨髄性およびリンパ性細胞におけるアポトーシスを抑制する.
- ニューロン細胞死におけるbcl-2の役割を理解することは不可欠です.
研究 の 目的:
- ニューロンのアポトーシスの予防におけるbcl-2の機能を調査する.
- ニューロントロフィック因子欠乏によって引き起こされる死亡からニューロンを救うことができるかどうかを判断する.
- 異なるニューロン死亡経路を特定するために.
主な方法:
- 胚性ニューロンにbcl-2発現ベクトルのマイクロインジェクション.
- アポトーシスを誘発するニューロトロフィック因子の剥奪.
- センサリーニューロンのシリアニューロトロフィック因子 (CNTF) への曝露.
主要な成果:
- bcl-2は,神経成長因子ファミリーのメンバーに依存する感覚神経細胞を救出しました.
- bcl-2は,シリアニューロントロフィック因子 (CNTF) に依存するシリアニューロンを救出しなかった.
- 感覚ニューロンは,CNTF曝露後にbcl-2に耐性を持つようになった.
結論:
- 少なくとも2つの異なる神経死経路が存在する.
- ニューロンアポトーシスのbcl-2への感受性は,関連する特定の神経栄養素因子に依存します.
- これらの発見は,神経細胞の生存と死亡の規制の複雑さを強調しています.
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