v-Src和EJ Ras减轻了细胞特异性抑制剂对c-Jun的抑制
V R Baichwal1, A Park, R Tjian
1Howard Hughes Medical Institute, University of California, Berkeley 94720.
Nature
|July 11, 1991
概括
像src和ras这样的原型瘤基因通过破坏其抑制剂来激活转录因子AP-1 (激活蛋白-1). 这种由瘤基因诱导的AP-1活性是由c-Jun激活域介导的.
科学领域:
- 分子生物学分子生物学
- 蜂信号传输是如何进行的
- 癌症研究 癌症研究
背景情况:
- 包括c-Jun和c-Fos在内的转录因子AP-1家族调节细胞基因和瘤基因表达.
- c-Jun的转录活性被一种细胞类型特定的抑制剂抑制,该抑制剂作用于其激活域 (A1) 和负调节区域 (delta).
研究的目的:
- 研究 src 和 ras 瘤基因增强c-Jun转录活性的机制.
- 为了确定参与基因介导刺激的c-Jun的特定区域.
主要方法:
- 通过GAL4:c-Jun混合结构对src或ras瘤基因的共感染.
- 评估具有或没有c-Jun抑制剂的细胞系中的转录活性.
主要成果:
- Src和ras瘤基因增强含有delta-A1区域的GAL4:c-Jun混合体的转录活性,独立于c-Jun的DNA结合和二元化域.
- 瘤基因诱导的c-Jun活性在具有抑制剂的细胞中被观察到,但在缺乏抑制剂的细胞中没有.
- c-Jun的A1域对于src和ras的刺激至关重要.
结论:
- Src和ras瘤基因刺激c-Jun和AP-1的转录活动.
- 这种刺激可能通过信号传导途径发生,这些途径会破坏c-Jun与其抑制剂之间的相互作用.
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