P2Y2 and TrkA receptors interact with Src family kinase for neuronal differentiation

被引：35

作者：

Arthur, David B. ^{[1
]}

Akassoglou, Katerina ^{[1
]}

Insel, Paul A. ^{[1
]}

机构：

[1] Univ Calif San Diego, Dept Pharmacol, La Jolla, CA 92093 USA

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2006年 / 347卷 / 03期

关键词：

NGF; dorsal root ganglion; PC12; nucleotide; neurite; NERVE GROWTH-FACTOR; PHEOCHROMOCYTOMA CELLS; TYROSINE KINASES; ACTIVATION; PROTOONCOGENE;

D O I：

10.1016/j.bbrc.2006.06.141

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

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.

引用

页码：678 / 682

页数：5

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