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NF-kappa Bのp50サブユニットの生成は,p105をATP依存の経路を通じて処理することによって行われる

C M Fan¹, T Maniatis

¹Department of Biochemistry and Molecular Biology, Harvard University, Cambridge, Massachusetts 02138.

|December 5, 1991

まとめ

NF-kappa B転写因子のサブユニットである機能的p50は,その前駆体であるp105.5のATP依存タンパク質分解によって生成されます. p105のC端領域は,処理後に分解され,細胞質複合体の組み立てに関与している可能性があります.

科学分野:

分子生物学は分子生物学である.
細胞生物学細胞生物学
バイオケミストリーバイオケミストリー

背景:

核因子カッパB (NF-カッパB) は,免疫反応と細胞プロセスに関与する重要な転写因子です.
NF-kappa Bは,p50およびp65サブユニットのヘテロダイマーとして機能します.
p50サブユニットは,より大きな前駆体であるp105から派生しているが,その生成のメカニズムとp105C末端の運命は不明であった.

研究の目的:

p105.5からp50生成のメカニズムを解明する.
p50生産中のp105のC端末領域の役割と運命を調査する.
NF-kappa B p105前駆体のインビボ処理を理解するために.

主な方法:

In vitro タンパク質翻訳でp105.5を生成する.
バイオケミカルアッセイを用いたタンパク質の加工と分解の分析.
ATP依存型タンパク質分解の研究.

主要な成果:

機能的なp50は,p105.pのATP依存タンパク質分解によって生成されます.
p105のC端半数は,この処理に欠かせない.
p105のC端領域は,p50生成後に急速に劣化しています.

結論:

ATP依存型タンパク質分解は,p105.5から活性p50サブユニットを生成する鍵となるメカニズムである.
処理後のp105のC端領域は,分解を対象としています.
p105のC末端領域は,イカッパB阻害剤を持つNF-カッパB複合体の細胞質組成に役割を果たす可能性がある.

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