Physiological function of voltage-dependent Na^+ channel β-subunit as an adhesion molecule
电压依赖性Na^+通道β亚基作为粘附分子的生理功能
基本信息
- 批准号:15500263
- 负责人:
- 金额:$ 2.43万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (C)
- 财政年份:2003
- 资助国家:日本
- 起止时间:2003 至 2004
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Voltage-dependent Na^+ channel β-subunits contain a single extracellular Ig-like domain with structural similarity to the cell adhesion molecules. In this project, we have studied the regulatory mechanisms of expression and intracellular trafficking of the β-subunits as well as their role in cell differentiation.In cultured bovine adrenal chromaffin cells, insulin and IGF-1 increased cell surface expression of Na^+ channels. Insulin and IGF-1 increased Na^+ channel α-subunit mRNA level but not (β-subunit mRNA level. In rat pheochromocytoma PC 12 cells, neuronal differentiation by nerve growth factor increased β_1-subunit mRNA level but not β_3-subunit mRNA level, indicating that the mechanisms regulating the expression of a-subunit and β-subunits are different.When HEK293 cells were transfected with GFP tagged β-subunit constructs, β_1-Subunit-GFP was expressed strongly at the cell surface and weakly in endoplasmic reticulum. β_2-Subunit-GFP was expressed predominantly at cell surface, and these cells extended many microvilli. β_3-Subunit-GFP was expressed strongly at cell membrane and at intracellular spherical membrane structure, and these cells also extended microvilli, indicating that the intracellular trafficking and the physiological function of the β-subunits are different. In addition, PC12 cells expressing each subunit tagged with GFP extended neuritis even in the absence of nerve growth factor, and the effects of β_2-GFP or β_3-GFP were stronger than that of β_1-GFP. The neurite extending effects of nerve growth factor were more pronounced in each β-subunit-GFP expressing cells than in the control cells.These results indicate that β-subunits play a role in the regulation of cell differentiation, and that the intracellular trafficking mechanisms of the β-subunits and their regulatory mechanisms of expression are different.
电压依赖性 Na^+ 通道 β 亚基包含单个细胞外 Ig 样结构域,其结构与细胞粘附分子相似。在本项目中,我们研究了β亚基的表达和细胞内运输的调控机制及其在细胞分化中的作用。在培养的牛肾上腺嗜铬细胞中,胰岛素和IGF-1增加了细胞表面Na^+通道的表达。胰岛素和IGF-1增加Na^+通道α亚基mRNA水平,但不增加β亚基mRNA水平。在大鼠嗜铬细胞瘤PC 12细胞中,神经生长因子向神经元分化增加β_1-亚基mRNA水平,但不增加β_3-亚基mRNA水平,表明调节a-亚基和β-亚基表达的机制不同。 HEK293细胞用GFP标记的β亚基构建体转染,β_1-亚基-GFP在细胞表面强表达,在内质网中弱表达。 β_2-亚基-GFP主要在细胞表面表达,这些细胞延伸出许多微绒毛。 β_3-亚基-GFP 在细胞膜和 细胞内呈球形膜结构,并且这些细胞还延伸出微绒毛,表明β亚基的细胞内运输和生理功能是不同的。此外,即使在没有神经生长因子的情况下,表达GFP标记的各亚基的PC12细胞也能产生延伸性神经炎,且β_2-GFP或β_3-GFP的作用强于β_2-GFP或β_3-GFP。 β_1-GFP。神经生长因子的神经突延伸作用在各β亚基-GFP表达细胞中均比对照细胞更明显。这些结果表明β亚基在细胞分化的调节中发挥作用,并且β亚基的细胞内运输机制及其表达调节机制是不同的。
项目成果
期刊论文数量(38)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Yanagita T. et al.: "Destabilization of sodium channel α-subunit mRNA by constitutive phosphrylation of ERK : Negatively regulation of steady-state level of cell surface functional sodium channels"Molecular Pharmacol.ogy. 63. 1125-1136 (2003)
Yanagita T.等人:“通过ERK的组成型磷酸化使钠通道α-亚基mRNA不稳定:细胞表面钠功能通道的稳态水平的负调节”《分子药理学》63. 1125-1136 (2003)。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Regulation of cell surface expression of voltage-dependent Nav1.7 sodium channels:: MRNA stability and posttranscriptional control in adrenal chromaffin cells
- DOI:10.2741/1314
- 发表时间:2004-05-01
- 期刊:
- 影响因子:3.1
- 作者:Wada, A;Yanagita, T;Kobayashi, H
- 通讯作者:Kobayashi, H
Molecular mechanisms and drug development in aquaporin water channel diseases : Aquaporin in the brain
水通道蛋白水通道疾病的分子机制和药物开发:大脑中的水通道蛋白
- DOI:
- 发表时间:2004
- 期刊:
- 影响因子:0
- 作者:横尾 宏毅 他;Yokoo H. et al.;Wada A.et al.;Kobayashi H. et al.;Yanagita T. et al.;Kobayashi H. et al.;Kobayashi H. et al.
- 通讯作者:Kobayashi H. et al.
Cell Biology of the Chromaffin Cells
嗜铬细胞的细胞生物学
- DOI:
- 发表时间:2004
- 期刊:
- 影响因子:0
- 作者:横尾 宏毅 他;Yokoo H. et al.;Wada A.et al.;Kobayashi H. et al.;Yanagita T. et al.;Kobayashi H. et al.;Kobayashi H. et al.;Shiraishi S. et al.;Yokoo H. et al.;Yanagita T. et al.;Kobayashi H. et al.;Yanagita T. et al.
- 通讯作者:Yanagita T. et al.
Pathophysiological function of adrenomedullin and proadrenomedullin N-terminal peptides in adrenal chromaffin cells.
- DOI:10.1291/hypres.26.s71
- 发表时间:2003-02
- 期刊:
- 影响因子:0
- 作者:Hideyuki Kobayashi;T. Yanagita;H. Yokoo;A. Wada
- 通讯作者:Hideyuki Kobayashi;T. Yanagita;H. Yokoo;A. Wada
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KOBAYASHI Hideyuki其他文献
KOBAYASHI Hideyuki的其他文献
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{{ truncateString('KOBAYASHI Hideyuki', 18)}}的其他基金
Elucidation of male infertility by epigenome analysis of iPS cells derived from male infertility and stem cell research
通过对源自男性不育症和干细胞研究的 iPS 细胞进行表观基因组分析来阐明男性不育症
- 批准号:
16K11072 - 财政年份:2016
- 资助金额:
$ 2.43万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
The breakthrough of male infertily by stem cell research
干细胞研究突破男性不育症
- 批准号:
24791674 - 财政年份:2012
- 资助金额:
$ 2.43万 - 项目类别:
Grant-in-Aid for Young Scientists (B)
Educational Visual Acuity Assessment of Children with Profound and Multiple Disabilities
重度和多重残疾儿童的教育视力评估
- 批准号:
22531070 - 财政年份:2010
- 资助金额:
$ 2.43万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Research of the business dispute resolution process from a viewpointof legal negotiation
法律谈判视角下的商事纠纷解决流程研究
- 批准号:
22530076 - 财政年份:2010
- 资助金额:
$ 2.43万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Identification and analysis of human spermatogonial stem cells
人精原干细胞的鉴定与分析
- 批准号:
20791127 - 财政年份:2008
- 资助金额:
$ 2.43万 - 项目类别:
Grant-in-Aid for Young Scientists (B)
Regulatory mechanisms of expression and localization of aquaporin water channels in brain microvessels
脑微血管中水通道蛋白水通道表达和定位的调控机制
- 批准号:
17590473 - 财政年份:2005
- 资助金额:
$ 2.43万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Method of the Training and Instruction in the Use of Optical Aids for Partial Sighted
弱视配镜使用训练及指导方法
- 批准号:
16530625 - 财政年份:2004
- 资助金额:
$ 2.43万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Regulatory mechanism of aquaporin expression in cerebral microvessels : its pathophysiological significance
脑微血管水通道蛋白表达的调控机制及其病理生理意义
- 批准号:
13672394 - 财政年份:2001
- 资助金额:
$ 2.43万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
相似国自然基金
工业用腈水合酶全新蛋白质翻译后调节体系self-subunit swapping的研究
- 批准号:31070711
- 批准年份:2010
- 资助金额:35.0 万元
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