Novel form of crosstalk between G protein and tyrosine kinase pathways
Novel form of crosstalk between G protein and tyrosine kinase pathways
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DOI：
10.1073/pnas.94.10.5417
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发表时间：
1997-05-13
影响因子：
11.1
通讯作者：
Dunlap, K
中科院分区：
文献类型：
--
作者：
DiversePierluissi, M;Remmers, AE;Dunlap, K
神经元 Ca2+ 通道受到多种与 G(o) 型 GTP 结合蛋白偶联的递质受体的抑制。据推测，G(o) 通过激活的 G 蛋白亚基和 Ca2+ 通道复合物之间的直接相互作用发挥作用。在这里，我们表明，γ-氨基丁酸产生的感觉神经元 N 型 Ca2+ 通道的抑制涉及一种由 G α(o) 和 src 样激酶介导的新型、快速激活的酪氨酸激酶信号通路。与最近描述的其他 G 蛋白偶联酪氨酸激酶途径相比，G α(o) 介导的调节既不需要蛋白激酶 C，也不需要细胞内 Ca2+。结果表明，该通路介导神经系统中的快速受体-G 蛋白信号传导，并支持 G 蛋白和酪氨酸激酶通路之间存在以前未被识别的串扰形式。
Neuronal Ca2+ channels are inhibited by a variety of transmitter receptors coupled to G(o)-type GTP-binding proteins. G(o) has been postulated to work via a direct interaction between an activated G protein subunit and the Ca2+ channel complex. Here we show that the inhibition of sensory neuron N-type Ca2+ channels produced by gamma-aminobutyric acid involves a novel, rapidly activating tyrosine kinase signaling pathway that is mediated by G alpha(o), and a src-like kinase. In contrast to other recently described G protein-coupled tyrosine kinase pathways, the G alpha(o)-mediated modulation requires neither protein kinase C nor intracellular Ca2+. The results suggest that this pathway mediates rapid receptor-G protein signaling in the nervous system and support the existence of a previously unrecognized form of crosstalk between G protein and tyrosine kinase pathways.