遺伝子的に定義された2つのトランス作用局は,肝臓特異的な遺伝子の重複するセットを協調的に調節します
S Ruppert1, M Boshart, F X Bosch
1Institute of Cell and Tumor Biology, German Cancer Research Center, Heidelberg.
Cell
|June 1, 1990
まとめ
マウスのアルフトランス作用因子の喪失は,新生児の肝機能を乱し,致死性を引き起こします. グルココルチコイドとcAMPは,この効果を逆転させ,alfとTse-1による調整された遺伝子調節を明らかにすることができます.
科学分野:
- 分子生物学は分子生物学である.
- 発達生物学 発達生物学について
- 遺伝学 遺伝学とは
背景:
- アルビノ位置の近くで欠損したマウスは,致命的な新生児現象型を示しています.
- このフェノタイプは,トランス作用因子,alf.の喪失と関連しています.
- 新生児の肝機能は,アルファ欠乏症のマウスで低下しています.
研究 の 目的:
- ALFトランス作用因子によって調節される遺伝子を特定する.
- アルファ媒介遺伝子発現におけるグルココルチコイドとcAMPの役割を調査する.
- alfと組織特異的な消火器の場所 Tse-1 の間の相互作用を探求する.
主な方法:
- アルフ反応性遺伝子を隔離するために差分cDNAスクリーニング.
- ホルモン刺激に反応する遺伝子発現パターンの分析.
- アルフ調節遺伝子に対するTse-1の効果を調査した.
主要な成果:
- 転写がalf.によって影響を受ける遺伝子を特定した.
- アルフ反応性遺伝子は,グルココルチコイドとcAMPによって誘発される.
- Tse-1がアルファ反応性遺伝子のサブセットを否定的に制御することを発見した.
- グルココルチコイドとcAMPがTse-1-媒介抑制を克服できることを実証しました.
結論:
- 2つのトランス作用因子,alfとTse-1は,肝臓特異的な遺伝子セットの重複の調節を調整する.
- 致死性フェノタイプと消滅した遺伝子発現は,ホルモン信号伝達経路の障害による可能性が高い.
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