2013 Fiscal Year Final Research Report
Regulation of ErbB4 via stimulation of GPCR for neurotransmitter and synaptic functions
Project/Area Number |
23500451
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Neurochemistry/Neuropharmacology
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Research Institution | University of the Ryukyus |
Principal Investigator |
YAMAMOTO Hideyuki 琉球大学, 医学(系)研究科(研究院), 教授 (60191433)
|
Co-Investigator(Kenkyū-buntansha) |
NAKAMINE Sayomi 琉球大学, 大学院・医学研究科, 助教 (20381105)
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Project Period (FY) |
2011 – 2013
|
Keywords | GT1-7細胞 / G蛋白質共役型受容体 / ゴナドトロピン放出ホルモン / ErbB4 / Gq/11蛋白質 / PKD / Fyn / 脱感作現象 |
Research Abstract |
ErbB4 belongs to the ErbB protein family and is abundantly expressed in neurons. It plays important roles in synaptic functions. In the previous work, we found that gonadotropin-releasing hormone (GnRH) transactivated ErbB4 in hypothalamic neurons (GT1-7 cells). We also found that the higher concentration of GnRH induced the cleavage of ErbB4. In the present study, we examined the molecular mechanisms of GnRH-induced activation and cleavage of ErbB4. ErbB4 activation was measured by the ErbB4-induced activation of ERK. We found that Gq/11 proteins, PKC, PKD, Fyn and PYK2 were involved in the activation of ErbB4. In contrast, only Gq/11 proteins and PKC, but not PKD, Fyn and PYK2, were involved in the cleavage of ErbB4. These results suggest that the activation and cleavage of ErbB4 are induced by different molecular mechanisms after PKC activation.
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Research Products
(31 results)