G protein-dependent vectorial transportation of receptors, ion channels, and transporters
受体、离子通道和转运蛋白的 G 蛋白依赖性载体运输
基本信息
- 批准号:12144202
- 负责人:
- 金额:$ 32.77万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research on Priority Areas
- 财政年份:2000
- 资助国家:日本
- 起止时间:2000 至 2004
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
G protein-coupled or tyrosine kinase-linked receptors are involved in the regulations of many signal transductions. After the stimulation of these membrane receptors, not only the receptor molecules themselves but also ion channels or transporters are internalized into the cells through endocytic pathways. Thus, there is vectorial transportation in the membrane trafficking. In this study, we investigated the molecular mechanisms whereby these receptors regulate the vectorial transportation.The major findings obtained in this study are summarized as follows.1) The lipid kinase phosphatidylinositol (PI) 3-OH kinase is synergistically stimulated by different types of membrane receptors, such as G protein-coupled and tyrosine kinase-linked receptors. We have found that the class I (p110beta subtype) PI 3-OH kinase is responsible for the synergistic stimulation and that its adaptor, Gab2, is involved in the signaling through its dual phosphorylation by Src tyrosine kinase and ERK. 2) The small GTPase Rab family are involved in membrane trafficking pathways. We have identified novel members of the RIN family as guanine nucleotide-exchange factors (GEFs) for Rab5. The RIN family, which contains many functional domains, such as SH2, Pro-rich region (binding to SH3), Vps9 (GEF), and RA (Ras-association), appear to act as adaptors or scaffold proteins in early steps of the endocytic pathway. 3) We have also identified novel family of Ras-like small GTPases, Di-Ras, Rheb, which might be involved in membrane trafficking pathways. Rheb expression in culture cells induced formation of the cytoplasmic large vacuoles, which are characterized as late endocytic (late endosome-and lysosome-like) components. Rheb appears to regulate the internalization of glutamate transporter in glial cells.
G蛋白偶联或酪氨酸激酶连接的受体参与许多信号转导的调节。在这些膜受体的刺激下,不仅受体分子本身,而且离子通道或转运体也通过内吞途径内化到细胞内。因此,在膜运输中存在着媒介运输。在本研究中,我们研究了这些受体调节载体转运的分子机制。主要研究结果如下:1)不同类型的膜受体,如G蛋白偶联受体和酪氨酸激酶连接受体,协同激活脂蛋白激酶磷脂酰肌醇(PI)3-OH激酶。我们发现I类(p110β亚型)PI3-OH激酶负责协同刺激,其接头Gab2通过Src酪氨酸激酶和ERK的双重磷酸化参与信号转导。2)小G蛋白转运酶Rab家族参与膜转运途径。我们已经确定RIN家族的新成员是Rab5的鸟嘌呤核苷酸交换因子(GEF)。RIN家族包含许多功能结构域,如SH2、Pro富集区(与SH3结合)、Vps9(环境基金)和RA(RAS结合),在内吞途径的早期阶段似乎扮演着接头或支架蛋白的角色。3)我们还发现了一个新的Ras样小GTP酶家族Di-Ras、Rheb,它们可能参与了膜转运途径。Rheb在培养细胞中的表达诱导了细胞质大空泡的形成,这些大空泡的特征是晚内吞(晚内吞体样和溶酶体样)成分。Rheb似乎调节神经胶质细胞中谷氨酸转运体的内化。
项目成果
期刊论文数量(115)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
K.Saito, J.Murai, H.Kajiho, K.Kontani, H.Kurosu, T.Katada: "A novel binding protein composed of homophilic tetramer exhibits unique properties for the small GTPase Rab5"J.Biol.Chem.. 277(in press). (2002)
K.Saito、J.Murai、H.Kajiho、K.Kontani、H.Kurosu、T.Katada:“由同亲四聚体组成的新型结合蛋白对小 GTPase Rab5 表现出独特的特性”J.Biol.Chem.. 277
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Activation of extracellular signal-regulated kinase by ultraviolet is mediated through Src-dependent epidermal growth factor receptor phosphorylation
紫外线激活细胞外信号调节激酶是通过 Src 依赖性表皮生长因子受体磷酸化介导的
- DOI:
- 发表时间:2002
- 期刊:
- 影响因子:0
- 作者:Kitajiri;S.;D.Kitagawa
- 通讯作者:D.Kitagawa
K.Kontani, M.Tada, T.Ogawa, T.Okai, K.Saito, Y.Araki, T.Katada: "Di-Ras : A distinct subgroup of Ras-family GTPases with unique biochemical properties"J.Biol.Chem.. 277. 41070-41078 (2002)
K.Kontani、M.Tada、T.Okawa、T.Okai、K.Saito、Y.Araki、T.Katada:“Di-Ras:具有独特生化特性的 Ras 家族 GTP 酶的独特亚组”J.Biol。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Ski7p G protein interacts with the exosome and the Ski complex for 3′-to-5′ mRNA decay in yeast
- DOI:10.1093/emboj/20.17.4684
- 发表时间:2001-09-03
- 期刊:
- 影响因子:11.4
- 作者:Araki, Y;Takahashi, S;Katada, T
- 通讯作者:Katada, T
Decapping reaction of mRNA requires Dcp1 in fission yeast: Its characterization in different species from yeast to human
- DOI:10.1093/jb/mvh190
- 发表时间:2004-12-01
- 期刊:
- 影响因子:2.7
- 作者:Sakuno, T;Araki, Y;Katada, T
- 通讯作者:Katada, T
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KATADA Toshiaki其他文献
KATADA Toshiaki的其他文献
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{{ truncateString('KATADA Toshiaki', 18)}}的其他基金
Identification of signaling pathways involved in fungal pathogenicity and search for novel targets for antifungal drugs
鉴定真菌致病性信号通路并寻找抗真菌药物新靶点
- 批准号:
20K06550 - 财政年份:2020
- 资助金额:
$ 32.77万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Nutrient response mediated by a TRIM-NHL protein
TRIM-NHL 蛋白介导的营养反应
- 批准号:
16K14693 - 财政年份:2016
- 资助金额:
$ 32.77万 - 项目类别:
Grant-in-Aid for Challenging Exploratory Research
A novel signal transduction pathway which regulates the structure of P-body and the dynamics of ARE-mRNAs
调节 P-body 结构和 ARE-mRNA 动态的新型信号转导途径
- 批准号:
22659015 - 财政年份:2010
- 资助金额:
$ 32.77万 - 项目类别:
Grant-in-Aid for Challenging Exploratory Research
Regulation of intracellular vesicle transport by small GTPase cycles
小 GTP 酶循环调节细胞内囊泡运输
- 批准号:
20247011 - 财政年份:2008
- 资助金额:
$ 32.77万 - 项目类别:
Grant-in-Aid for Scientific Research (A)
Membrane-Transport Signaling Involving the GTPase Cycle of G proteins
涉及 G 蛋白 GTP 酶循环的膜运输信号转导
- 批准号:
18207008 - 财政年份:2006
- 资助金额:
$ 32.77万 - 项目类别:
Grant-in-Aid for Scientific Research (A)
Functional analysis of atypical G proteins involved in cell signaling network
参与细胞信号网络的非典型G蛋白的功能分析
- 批准号:
17079002 - 财政年份:2005
- 资助金额:
$ 32.77万 - 项目类别:
Grant-in-Aid for Scientific Research on Priority Areas
New research initiatives in the study of G-protein signaling systems integrating cell communication network
整合细胞通讯网络的G蛋白信号系统研究新举措
- 批准号:
17079001 - 财政年份:2005
- 资助金额:
$ 32.77万 - 项目类别:
Grant-in-Aid for Scientific Research on Priority Areas
The structure and function of a novel G protein family regulating eukaryotic mRNA dynamics
调节真核mRNA动态的新型G蛋白家族的结构和功能
- 批准号:
13854025 - 财政年份:2001
- 资助金额:
$ 32.77万 - 项目类别:
Grant-in-Aid for Scientific Research (S)
Physiological roles of cell surface ecto-enzymes
细胞表面胞外酶的生理作用
- 批准号:
11694249 - 财政年份:1999
- 资助金额:
$ 32.77万 - 项目类别:
Grant-in-Aid for Scientific Research (B).
Analysis of the functions of G protein βγ-Subunit and application to drug design
G蛋白βγ亚基的功能分析及其在药物设计中的应用
- 批准号:
10557220 - 财政年份:1998
- 资助金额:
$ 32.77万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
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