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ダブルトランスフォーメーションされたチキンミエロモノサイト細胞におけるv-mybのv-mycに対する優位性
1Differentiation Programme, European Molecular Biology Laboratory, Heidelberg, Federal Republic of Germany.
Cell
|October 9, 1987
まとめ
腫瘍遺伝子のv-mybは,鶏肉のミエロモノサイト細胞のv-mycを覆し,分化を停止する. v-mycは増殖を促進するが,v-mybは増殖を誘発し,細胞の分化を阻害する.
科学分野:
- 分子生物学は分子生物学である.
- 腫瘍学 腫瘍学
- 細胞の微分化は
背景:
- v-myc腫瘍遺伝子は,鶏肉のミエロモノサイト細胞を成熟したマクロファージに変換する.
- 逆に,v-mybまたはv-myb,etsの腫瘍遺伝子は,これらの細胞に未熟な現象型を誘導する.
研究 の 目的:
- 細胞変換におけるv-mycおよびv-myb腫瘍遺伝子の相互作用と優位性を調査する.
- v-mycとv-mybまたはv-myb,etsの共同発現が差異化現象型を変更するかどうかを判断する.
主な方法:
- チークミエロモノサイト細胞のv-mycおよびv-mybまたはv-myb,etsとの共変異.
- 細胞のフェノタイプとタンパク質発現を二重変異した細胞で分析する.
主要な成果:
- 二重変異細胞は,v-mybまたはv-myb,etsだけで変異された細胞とフェノタイプ的に同一であった.
- 高v-mycタンパク質発現は,v-myb.によって誘発されたフェノタイプを変更しませんでした.
- v-mybは,細胞の分化制御において,v-mycよりも優位性を示した.
結論:
- v-mybは,ミエロモノサイト細胞の分化を調節する際にv-mycよりも優位である.
- v-mycは,分化に影響を与えることなく細胞増殖を促します.
- v-mybは,増殖を誘導し,標的細胞の分化を阻害または逆転させます.
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