The dopamine D4 receptor activates intracellular platelet-derived growth factor receptor β to stimulate ERK1/2

被引：13

作者：

Gill, Robin S. ^{[1
]}

Hsiung, Marilyn S. ^{[1
,3
]}

Sum, Chi S. ^{[1
]}

Lavine, Natalie ^{[1
,3
]}

Clark, Stewart D. ^{[1
]}

Van Tol, Hubert H. M. ^{[1
,2
,3
,4
,5
]}

机构：

[1] Ctr Addict & Mental Hlth, Mol Neurobiol Lab, Toronto, ON M5T 1R8, Canada

[2] Univ Toronto, Dept Psychiat, Toronto, ON, Canada

[3] Univ Toronto, Dept Pharmacol, Toronto, ON, Canada

[4] Univ Toronto, Dept Physiol, Toronto, ON, Canada

[5] Univ Toronto, Inst Med Sci, Toronto, ON M5S 1A1, Canada

来源：

CELLULAR SIGNALLING | 2010年 / 22卷 / 02期

基金：

加拿大自然科学与工程研究理事会; 加拿大健康研究院;

关键词：

Dopamine; Platelet-derived growth factor; Transactivation; G protein-coupled receptor; PROTEIN-KINASE-C; TYROSINE KINASE; TRANSACTIVATION; DEGRADATION; PDGF; D-4; MEDIATE; SURFACE;

D O I：

10.1016/j.cellsig.2009.09.031

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Dopamine receptors are GPCRs that play important roles in locomotion, reward, and cognitive processes. Previously, we demonstrated that this receptor transactivates PDGFR beta to modulate ERK1/2 and NMDA receptor activity. Downregulation of maturely glycosylated PDGFR beta by prolonged exposure to PDGF-BB eliminated PDGF-BB-mediated ERK1/2 activation. The DRD4-mediated ERK1/2 response was only partially blunted by PDGF-BB-mediated downregulation, but remained sensitive to the PDGFW kinase inhibitor tyrphostin A9. Tunicamycin prevented the N-linked glycosylation and maturation of PDGFR beta as well as its activation by PDGF-BB. However, upon tunicamycin treatment, DRD4 continued to signal to ERK1/2 in a tyrphostin A9-sensitive manner. Collectively, our observations indicate that DRD4, unlike PDGF-BB, can activate a pool of intracellularly located PDGFR beta. (C) 2009 Elsevier Inc. All rights reserved.

引用

页码：285 / 290

页数：6

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