Functional analysis of the BRAG3-Arf6 pathway in the inhibitory synapse

抑制性突触中 BRAG3-Arf6 通路的功能分析

• 批准号: 22300114
• 负责人: SAKAGAMI Hiroyuki
• 金额: $ 11.32万
• 依托单位: Kitasato University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (B)
• 财政年份: 2010
• 资助国家: 日本
• 起止时间: 2010-04-01 至 2014-03-31
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-22300114/
• 关键词: 抑制性シナプス; 低分子量GTP結合タンパク質; シナプス後肥厚部; 足場タンパク質; シナプス可塑性; 低分子量GTP結合蛋白質; 低分子量G蛋白質; 細胞骨格; 神経可塑性; GABA; グリシン; 樹状突起

The aim of this study is to provide anatomincal evidence for the BRAG3-Arf6 pathway as a novel regulator of membrane traffic and actin cytoskeleton in the inhibitory synapse. First, we immunohistochemically demonstrated that BRAG3 localizes preferentially at postsynaptic specializations of symmetric synapses. Using yeast two-hybrid and pull down assays, we identified that BRAG3 can interact with utrophin/dystrophin and S-SCAM/MAGI-2, scaffolding proteins that localize at inhibitory synapses. Taken together, these findings suggest that BRAG3 may regulate the membrane traffic and actin cytoskeleton at inhibitory synapses through the interaction with scaffold proteins such as dystrophin and S-SCAM.

本研究的目的是为 BRAG3-Arf6 通路作为抑制性突触中膜交通和肌动蛋白细胞骨架的新型调节剂提供解剖学证据。首先，我们通过免疫组织化学证明 BRAG3 优先定位于对称突触的突触后特化。使用酵母双杂交和下拉分析，我们发现 BRAG3 可以与肌养蛋白/肌营养不良蛋白和 S-SCAM/MAGI-2（定位于抑制性突触的支架蛋白）相互作用。总而言之，这些发现表明 BRAG3 可能通过与肌营养不良蛋白和 S-SCAM 等支架蛋白的相互作用来调节抑制性突触的膜交通和肌动蛋白细胞骨架。

项目成果

Endosomal localization of FIP3/Arfophilin-1 and its involvement in dendritic formation of mouse hippocampal neurons.

FIP3/Arfophilin-1 的内体定位及其参与小鼠海马神经元树突形成。

• DOI: 10.1016/j.brainres.2014.02.018
• 发表时间: 2014
• 影响因子: 2.9
• 作者: Yazaki Y; Hara Y; Tamaki H; Fukaya M; Sakagami H.
• 通讯作者: Sakagami H.

Vascular endothelial growth factor receptor-1 signalingpromotes liver repair through restoration of liver microvasculature afteracetaminophen hepatotoxicity

对乙酰氨基酚肝毒性后血管内皮生长因子受体-1信号传导通过恢复肝脏微血管系统促进肝脏修复

• DOI: 10.1093/toxsci/kfq366
• 发表时间: 2011
• 影响因子: 3.8
• 作者: Kato T; Ito Y; Hosono K; Suzuki T; Tamaki H; Minamino T; Kato S; Sakagami H; Shibuya M; Majima M
• 通讯作者: Majima M

SynArfGEF is a guanine nucleotide exchage factor for Arf6 and localizes preferentially at post-synaptic specialization of inhibitory synapses.

SynArfGEF 是 Arf6 的鸟嘌呤核苷酸交换因子，优先定位于抑制性突触的突触后特化。

• 发表时间: 2011
• 影响因子: 4.7
• 作者: Fukaya M; Kamata A; Hara Y; Tamaki H; Katsumata O; Ito N; Takeda S; Hata Y; Suzuki T; Watanabe M; Harvey RJ; Sakagami H.
• 通讯作者: Sakagami H.

Involvement of the serum response factor coactivator megakaryoblastic leukemia (MKL) in the activin-regulated dendritic complexity of rat cortical neurons

血清反应因子共激活因子巨核细胞白血病（MKL）参与激活素调节的大鼠皮质神经元树突复杂性

• DOI: 10.1074/jbc.m110.118745
• 发表时间: 2010
• 影响因子: 4.8
• 作者: Ishikawa M; Nishijima N; Shiota J; Sakagami H; Tsuchida K; Mizukoshi M; Fukuchi M; Tsuda M; Tabuchi A
• 通讯作者: Tabuchi A

USP9x-mediated deubiquitination of EFA6 regulates de novo tight junction assembly.

USP9x 介导的 EFA6 去泛素化从头调节紧密连接组装。

• 发表时间: 2010
• 影响因子: 11.4
• 作者: Theard D; Labarrade F; Partisani M; Milanini J; Sakagami H; et al.
• 通讯作者: et al.