Oncogenic kinase signalling

被引：2984
作者：
Blume-Jensen, P [1 ]
Hunter, T [1 ]
机构：
[1] Salk Inst Biol Studies, Mol & Cell Biol Lab, La Jolla, CA 92037 USA
来源：
NATURE | 2001年 / 411卷 / 6835期
关键词：
D O I：
10.1038/35077225
中图分类号：
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
Protein-tyrosine kinases (PTKs) are important regulators of intracellular signal-transduction pathways mediating development and multicellular communication in metazoans. Their activity is normally tightly controlled and regulated. Perturbation of PTK signalling by mutations and other genetic alterations results in deregulated kinase activity and malignant transformation. The lipid kinase phosphoinositide 3-OH kinase (PI(3)K) and some of its downstream targets, such as the protein-serine/threonine kinases Akt and p70 S6 kinase (p70(S6K)), are crucial effectors in oncogenic PTK signalling. This review emphasizes how oncogenic conversion of protein kinases results from perturbation of the normal autoinhibitory constraints on kinase activity and provides an update on our knowledge about the role of deregulated PI(3)K/Akt and mammalian target of rapamycin/p70(S6K) signalling in human malignancies.
引用
收藏
页码：355 / 365
页数：11
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