瘤性激酶信号传递器
1The Salk Institute, Molecular and Cell Biology Laboratory, 10010 North Torrey Pines Road, La Jolla, California 92037, USA. blume@salk.edu
Nature
|May 18, 2001
概括
蛋白氨酸激酶 (PTKs) 调节细胞信号,但它们的放松调节会导致癌症. 本综述详细介绍了异常PI(3)K/Akt和mTOR/p70S6K通路如何导致人类恶性瘤.
科学领域:
- 分子生物学分子生物学
- 细胞信号传递 细胞信号传递
- 在瘤学瘤学.
背景情况:
- 蛋白氨酸激酶 (PTKs) 对于细胞通信和发育至关重要.
- 通常,PTK活动受到严格管制;失调导致恶性转变.
- 关键的下游效应体包括酸胺3-OH激酶 (PI(3) K) 和Akt/p70S6K.
研究的目的:
- 审查瘤性PTK如何从被破坏的自身抑制控制中产生.
- 更新关于人类癌症中不受管制的PI(3)K/Akt和mTOR/p70S6K信号的知识.
主要方法:
- 对PTK信号通路的文献综述.
- 对影响激酶活性的基因变异的分析.
- 专注于癌症中的PI(3)K/Akt和mTOR/p70S6K通路.
主要成果:
- 瘤性PTKs是由于正常自身抑制的丧失而产生的.
- 放松PI(3)K/Akt信号的调节是癌症中常见的机制.
- 异常的mTOR/p70S6K信号传递也对恶性瘤有很大的贡献.
结论:
- 了解PTK放松调节对于癌症治疗至关重要.
- 针对PI(3) K/Akt和mTOR/p70S6K通路提供了治疗潜力.
- 癌症治疗需要对激酶调节进行进一步的研究.
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