'Location, location, location': activation and targeting of MAP kinases by G protein-coupled receptors
'Location, location, location': activation and targeting of MAP kinases by G protein-coupled receptors
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DOI：
10.1677/jme.0.0300117
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发表时间：
2003-04-01
影响因子：
3.5
通讯作者：
Luttrell, LM
中科院分区：
文献类型：
--
作者：
Luttrell, LM
越来越多的数据支持G蛋白偶联受体可以通过控制MAP激酶的活性来调节细胞生长和分化的结论。异源三聚体G蛋白池的激活启动导致MAP激酶激活的复杂信号网络，其经常涉及G蛋白偶联受体和受体酪氨酸激酶之间的串扰或粘着斑。MAP激酶激活的主要机制在受体和细胞类型之间显著不同。此外，MAP激酶激活的机制对MAP激酶功能有实质性影响。一些信号导致活化的MAP激酶靶向特定的细胞核位置，而另一些信号则激活MAP激酶库，该激酶库可自由易位至细胞核并有助于促有丝分裂反应。
A growing body of data supports the conclusion that G protein-coupled receptors can regulate cellular growth and differentiation by controlling the activity of MAP kinases. The activation of heterotrimeric G protein pools initiates a complex network of signals leading to MAP kinase activation that frequently involves cross-talk between G protein-coupled receptors and receptor tyrosine kinases or focal adhesions. The dominant mechanism of MAP kinase activation varies significantly between receptor and cell type. Moreover, the mechanism of MAP kinase activation has a substantial impact on MAP kinase function. Some signals lead to the targeting of activated MAP kinase to specific extranuclear locations, while others activate a MAP kinase pool that is free to translocate to the nucleus and contribute to a mitogenic response.