M-CSF受容体の発現は,GM-CSFまたはマルチ-CSFの支配的な作用によって,転写後の制御されます
B C Gliniak1, L R Rohrschneider
1Fred Hutchinson Cancer Research Center, Seattle, Washington 98104.
Cell
|November 30, 1990
まとめ
グラヌロサイト・マクロファージ・コロニー刺激因子 (GM-CSF) とマルチコロニー刺激因子 (multi-CSF) は,骨髄性前駆細胞の発達を抑制する. この抑制はトランスクリプション後に行われ,c-fmsの発現と系統の制限に影響を与えます.
科学分野:
- ヘマトポエーシス (血液形成) とは
- 細胞シグナリング
- 分子生物学は分子生物学である.
背景:
- マウリンのミエロイド前駆細胞系FDC-P1/MACは,マルチ-CSF,GM-CSF,M-CSF (c-fmsプロトオンコゲン) の受容体を発現している.
- c-fms mRNAとタンパク質の発現はM-CSFでは高いが,マルチ-CSFまたはGM-CSFでは低下する.
研究 の 目的:
- ミエロイド成長因子によるc-fms発現の転写後の調節を調査する.
- GM-CSFとマルチ-CSFのミエロイド系統への影響を決定する.
主な方法:
- 成長因子研究のためにFDC-P1/MAC細胞系を利用した.
- c-fmsトランスクリプションを評価するための核ランオフアッセイを実施しました.
- 優位性を分析するために因子交換実験を行った.
- 骨髄細胞を用いたインビトロアガーアッセイで用いられる.
主要な成果:
- c-fmsの転写は成長因子とは無関係であり,規制は転写後のものです.
- マルチ-CSFとGM-CSFは,濃度に依存した方法でc-fms発現を圧倒的に抑制します.
- GM-CSFは,M-CSFの存在下でも,モノサイト/マクロファージの発達を防ぐことができます.
結論:
- GM-CSFとマルチ-CSFは,モノサイト/マクロファージの系統開発を抑制する.
- 成長因子シグナル伝達を含むストキャスティックメカニズムが,骨髄性系統の制限を統制する.
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