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Cell signaling by receptor tyrosine kinases

机译:受体酪氨酸激酶的细胞信号转导

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摘要

Recent structural studies of receptor tyrosine kinases (RTKs) have revealed unexpected diversity in the mechanisms of their activation by growth factor ligands. Strategies for inducing dimerization by ligand binding are surprisingly diverse, as are mechanisms that couple this event to activation of the intracellular tyrosine kinase domains. As our understanding of these details becomes increasingly sophisticated, it provides an important context for therapeutically countering the effects of pathogenic RTK mutations in cancer and other diseases. Much remains to be learned, however, about the complex signaling networks downstream from RTKs and how alterations in these networks are translated into cellular responses.
机译:受体酪氨酸激酶(RTK)的最新结构研究表明,其被生长因子配体激活的机制具有出乎意料的多样性。通过配体结合诱导二聚化的策略令人惊讶地多样,以及将这一事件与细胞内酪氨酸激酶结构域激活偶联的机制。随着我们对这些细节的理解变得越来越复杂,它为治疗性抵抗致病性RTK突变在癌症和其他疾病中的作用提供了重要的背景。但是,关于RTK下游的复杂信令网络以及如何将这些网络中的更改转换为蜂窝响应,还有很多事情要学习。

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