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タイトル: RasGRF1 mediates brain-derived neurotrophic factor-induced axonal growth in primary cultured cortical neurons
著者: Umeda, Kentaro
Negishi, Manabu
Katoh, Hironori
著者名の別形: 梅田, 健太郎
根岸, 学
加藤, 裕教
キーワード: Brain-derived neurotrophic factor
R-Ras
RasGRF1
Axon
発行日: Mar-2019
出版者: Elsevier BV
誌名: Biochemistry and Biophysics Reports
巻: 17
開始ページ: 56
終了ページ: 64
抄録: The appropriate development and regulation of neuronal morphology are important to establish functional neuronal circuits and enable higher brain function of the central nervous system. R-Ras, a member of the Ras family of small GTPases, plays crucial roles in the regulation of axonal morphology, including outgrowth, branching, and guidance. GTP-bound activated R-Ras reorganizes actin filaments and microtubules through interactions with its downstream effectors, leading to the precise control of axonal morphology. However, little is known about the upstream regulatory mechanisms for R-Ras activation in neurons. In this study, we found that brain-derived neurotrophic factor (BDNF) has a positive effect on endogenous R-Ras activation and promotes R-Ras-mediated axonal growth. RNA interference knockdown and overexpression experiments revealed that RasGRF1, a guanine nucleotide exchange factor (GEF) for R-Ras, is involved in BDNF-induced R-Ras activation and the promotion of axonal growth. Phosphorylation of RasGRF1 by protein kinase A at Ser916/898 is needed for the full activation of its GEF activity and to facilitate Ras signaling. We observed that BDNF treatment markedly increased this phosphorylation. Our results suggest that BDNF is one of the critical extrinsic regulators for R-Ras activation, and that RasGRF1 is an intrinsic key mediator for BDNF-induced R-Ras activation and R-Ras-mediated axonal morphological regulation.
著作権等: © 2018 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/BY-NC-ND/4.0/).
URI: http://hdl.handle.net/2433/235670
DOI(出版社版): 10.1016/j.bbrep.2018.11.011
出現コレクション:学術雑誌掲載論文等

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