P2Y2 and TrkA receptors interact with Src family kinase for neuronal differentiation
P2Y2 and TrkA receptors interact with Src family kinase for neuronal differentiation
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DOI：
10.1016/j.bbrc.2006.06.141
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发表时间：
2006-09-01
影响因子：
3.1
通讯作者：
Insel, Paul A.
中科院分区：
文献类型：
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作者：
Arthur, David B.;Akassoglou, Katerina;Insel, Paul A.
P2 Y（2）G蛋白偶联受体（GPCR）与TrkA受体酪氨酸激酶（RTK）之间的相互作用是调节神经元分化的重要机制。我们发现Src家族激酶（SFK）调节P2 Y（2）-TrkA分子串扰。SFK抑制剂阻断ATP γ S/P2 Y（2）促进的PC 12细胞中NGF/TrkA信号传导和神经元分化的增强，消除ATP γ S促进的背根神经节神经元原代培养物中轴突生长的增强，并阻断TrkA、P2 Y（2）受体和SFK的免疫共沉淀。这些结果确定SFK作为介导核苷酸增强的神经营养因子依赖性神经元分化，因此，作为RTK和GPCR之间相互作用的关键汇聚点。(c)2006年爱思唯尔公司All rights reserved.
The crosstalk between the P2Y(2) G-protein-coupled receptor (GPCR) with TrkA receptor tyrosine kinase (RTK) is an important mechanism that regulates neuronal differentiation. We show that Src family kinases (SFK) regulate P2Y(2)-TrkA molecular crosstalk. SFK inhibitors block ATP gamma S/P2Y(2)-promoted enhancement of NGF/TrkA signaling and neuronal differentiation in PC12 cells, abrogate the enhancement by ATP gamma S of neurite outgrowth in primary cultures of dorsal root ganglion neurons, and block co-immunoprecipitation of TrkA, P2Y(2) receptors and SFK. These results identify SFK as mediating nucleotide-enhanced neurotrophin-dependent neuronal differentiation and thus, as a key convergence point for interaction between RTKs and GPCRs. (c) 2006 Elsevier Inc. All rights reserved.