The dopamine D4 receptor activates intracellular platelet-derived growth factor receptor β to stimulate ERK1/2 |
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| Authors: | Robin S Gill Marilyn S Hsiung Chi S Sum Natalie Lavine Stewart D Clark Hubert HM Van Tol |
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| Institution: | 1. The Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, TX, USA;2. State Key Laboratory of Space Medicine Fundamentals and Application, China Astronaut Research and Training Center, Beijing, China;3. School of Life Science and Technology, Harbin Institute of Technology, Harbin, China;4. Department of Anesthesiology, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China;1. Sakarya University, Faculty of Medicine, Department of Pharmacology, 54100 Sakarya, Turkey;2. Kocaeli University, Faculty of Medicine, Department of Pharmacology, 41380 Kocaeli, Turkey;1. Sakarya University, Faculty of Medicine, Department of Pharmacology, 54100-Sakarya, Turkey;2. Kocaeli University, Faculty of Medicine, Department of Pharmacology, 41380-Kocaeli, Turkey |
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| Abstract: | Dopamine receptors are GPCRs that play important roles in locomotion, reward, and cognitive processes. Previously, we demonstrated that this receptor transactivates PDGFRβ to modulate ERK1/2 and NMDA receptor activity. Downregulation of maturely glycosylated PDGFRβ 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 PDGFRβ kinase inhibitor tyrphostin A9. Tunicamycin prevented the N-linked glycosylation and maturation of PDGFRβ 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 PDGFRβ. |
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