细胞转化和pp60c-src的激活通过蛋白质氨酸酸酶的过度表达
X M Zheng1, Y Wang, C J Pallen
1Cell Regulation Laboratory, National University of Singapore.
Nature
|September 24, 1992
概括
过度表达蛋白氨酸酸酶α (PTPα) 持续激活pp60c-src激酶,导致细胞转化和瘤发生. 这种激活涉及消极调节部位Tyr527.7的脱化.
科学领域:
- 细胞生物学 细胞生物学
- 分子瘤学分子瘤学
- 信号传输 信号传输
背景情况:
- pp60c-src激酶活性在细胞周期期间受到严格调节,通常在线粒分裂过程中增加.
- pp60c-src的失调,通常是通过突变或病毒coproteins,导致不受控制的细胞生长和癌症.
- 碳氧终端Tyr527位点对于负调节pp60c-src激酶活性至关重要.
研究的目的:
- 研究蛋白氨酸酸酶α (PTPα) 在调节pp60c-src激酶活性中的作用.
- 确定PTPα过度表达是否可以诱导细胞转化和瘤发生.
- 阐明 PTPα 影响 pp60c-src 活动的机制.
主要方法:
- 在细胞中过度表达PTPα.
- 评估pp60c-src激酶活性.
- 分析Tyr527.7的酸化状态.
- 通过使用纯化的PTPα进行体外去化试验.
主要成果:
- 过度表达PTPα导致了pp60c-src激酶的持续激活.
- 过度表达PTPα导致细胞转化和瘤发生.
- 在PTPα过度表达细胞中的pp60c-src激活与Tyr527.7.的脱化有关.
- 纯化的PTPα在体外直接去化Tyr527的pp60c-src.
结论:
- PTPα在调节细胞增殖方面发挥着重要作用.
- PTPα至少部分通过激活pp60c-src激酶来发挥其作用.
- 过度表达PTPα具有致癌能力,通过pp60c-src激活促进瘤发生.
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