The Cytophamacological Study on the Responses of the Receptors in the Cell System

细胞系统受体反应的细胞病理学研究

基本信息

  • 批准号:
    02454139
  • 负责人:
  • 金额:
    $ 3.97万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for General Scientific Research (B)
  • 财政年份:
    1990
  • 资助国家:
    日本
  • 起止时间:
    1990 至 1992
  • 项目状态:
    已结题

项目摘要

When the extracellular signals such as hormones, neurotransmitters, growth factors and so on reach the plasma membranes of the cells, a variety of active substances are produced in the cells. Calcium ion (Ca^<2+>) is now considered to be one of so called second messengers and involved in many physiological and pathophysiological processes of the living systems. The effects of Ca^<2+> in the cells may at least partly be mediated by Ca^<2_>/calmodulin-dependent protein kinase II (CaM kinase II). CaM kinase II is present at the highest concentration in the brain and undergoes autophosphorylation in the presence of Ca^<2+>/CaM. The autophosphorylation renders the enzyme Ca^<2+>-independent and is therefore considered to be the activation of the enzyme. In the present study, the activation of the enzyme was examined using the cultured cells such as the primary culture of neurons and the established cell lines such as PC12 cells, neuro-2A, 3Y1 cell, C6 gliona cell and NG108-15 cell. The isoe … More nzyme of CaM kinase II in NG108-15 cells were extensively studied. The Ca^<2+>/CaM-independent activity (autonomous activity) of the enzyme increased twice within 10 sec by stimulation with 1 muM bradykinin in the cells. The increase in the autonomous activity of the enzyme had two phases; the transient early-peak phase and the long late-plateau phase. The former was abolished by the pretreatment of the cells with 10 mM caffeine or 20 muM BAPTA-AM, and the latter was abolished by the removal of the extracellular Ca^<2+> with 1 mM EGTA or by the pretreatment with 1 muM nifedipine. Stimulation of ^<32>P-labeled NG108-15 cells with 1 muM bradykinin increased the autophosphorylation of CaM kinase II and this increase was abolished by pretreatment with caffeine or BAPTA-AM. These results suggest that CaM kinase II is activated via the inositol phospholipid signaling pathway induced with bradykinin in NG108-15 cells. Thus we were able to show the change in the enzyme activity in response to the drugs in intact cells, which was coupled to the Ca^<2+> mobilization. Less
当激素、神经递质、生长因子等细胞外信号到达细胞质膜时,细胞内产生多种活性物质。钙离子(Ca^<2+>)被认为是第二信使之一,参与生命系统的许多生理和病理生理过程。Ca^2+在细胞中的作用可能至少部分由Ca^2<2_>/钙调蛋白依赖性蛋白激酶II(CaM激酶II)介导。CaM激酶II在脑中的浓度最高,在Ca^&lt;2+&gt;/CaM存在时发生自磷酸化。自磷酸化使酶不依赖于Ca^2+,因此被认为是酶的活化。在本研究中,使用培养的细胞如神经元的原代培养物和建立的细胞系如PC 12细胞、neuro-2A、3 Y1细胞、C6胶质瘤细胞和NG 108 -15细胞检测酶的活化。isoe ...更多信息 对NG 108 -15细胞中CaM激酶Ⅱ的酶活性进行了研究。用1 μ M缓激肽刺激细胞,10秒内酶的Ca^&lt;2+&gt;/CaM非依赖性活性(自主活性)增加两倍。该酶的自主活性的增加有两个阶段;短暂的早期峰值阶段和长期的后期平台阶段。用10 mM咖啡因或20 μ M BAPTA-AM预处理细胞可消除前者,用1 mM EGTA去除细胞外Ca^&lt;2+&gt;或用1 μ M硝苯地平预处理细胞可消除后者。用<32>1 μ M缓激肽刺激13 P标记的NG 108 -15细胞,可增加CaM激酶II的自磷酸化,这种增加可被咖啡因或BAPTA-AM预处理所消除。这些结果表明,钙调蛋白激酶II激活通过肌醇磷脂信号通路诱导缓激肽在NG 108 -15细胞。因此,我们能够显示完整细胞中酶活性对药物的反应变化,这与Ca^2+动员有关。少

项目成果

期刊论文数量(47)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
T.Yamakawa: "Activation of Ca^<2+>/calmodulin-dependent protein kinase II by stimulation with bradykinin in neuroblastoma × glioma hybrid NG108-15 cells." Brain Res.597. 220-226 (1992)
T. Yamakawa:“通过在神经母细胞瘤 × 神经胶质瘤杂交 NG108-15 细胞中刺激 Ca^2+/钙调蛋白依赖性蛋白激酶 II”(Brain Res.597)。
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  • 影响因子:
    0
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  • 通讯作者:
Masami Takahashi: "Protein kinase C and Ca^<2+>/calmodulinーdependent protein kinase II phosphorylate a novel 58ーkDa protein in synaptic vesicles" Brain Research. 551. 279-292 (1991)
Masami Takahashi:“蛋白激酶 C 和 Ca^2+/钙调蛋白依赖性蛋白激酶 II 磷酸化突触小泡中的新型 58-kDa 蛋白”Brain Research 551. 279-292 (1991)。
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  • 发表时间:
  • 期刊:
  • 影响因子:
    0
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  • 通讯作者:
宮本 英七: "細胞系におけるCa^<2+>/カルモデュリン依存性プロテインキナ-ゼIIの細胞刺激に反応した調節" 日本薬理学雑誌. 98. 177-185 (1991)
Eishichi Miyamoto:“细胞系统中Ca 2+ /钙调蛋白依赖性蛋白激酶II响应于细胞刺激的调节”日本药理学杂志98。177-185(1991)。
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  • 发表时间:
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  • 影响因子:
    0
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B.A.Perrino: "Characterization of the phosphatase activity of a baculovirus-expressed calcineurin A isoform." J.Biol.Chem.267. 15965-15969 (1992)
B.A.Perrino:“杆状病毒表达的钙调神经磷酸酶 A 亚型的磷酸酶活性的表征。”
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    0
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MIYAMOTO Eishichi其他文献

MIYAMOTO Eishichi的其他文献

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{{ truncateString('MIYAMOTO Eishichi', 18)}}的其他基金

Establishment of cell models on transfection of functional protein and the study on brain signal transduction
功能蛋白转染细胞模型的建立及脑信号转导研究
  • 批准号:
    12557011
  • 财政年份:
    2000
  • 资助金额:
    $ 3.97万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Molecular and cytobiological study on regulation of synapse
突触调控的分子和细胞生物学研究
  • 批准号:
    11694295
  • 财政年份:
    1999
  • 资助金额:
    $ 3.97万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B).
Molecular cytobiological study on hippocampal LTP and LTD
海马LTP和LTD的分子细胞生物学研究
  • 批准号:
    09044324
  • 财政年份:
    1997
  • 资助金额:
    $ 3.97万
  • 项目类别:
    Grant-in-Aid for international Scientific Research
Molecular cytobiological study on CaィイD12+ィエD1 signaling in the cells with cultured cells
培养细胞中CaiD12+CaiD1信号传导的分子细胞生物学研究
  • 批准号:
    09480223
  • 财政年份:
    1997
  • 资助金额:
    $ 3.97万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Study on the mechanism of brain plasticity
脑可塑性机制研究
  • 批准号:
    07044281
  • 财政年份:
    1995
  • 资助金额:
    $ 3.97万
  • 项目类别:
    Grant-in-Aid for international Scientific Research
Intracellular responses by stimulation of receptors in neurons and related cells
通过刺激神经元和相关细胞中的受体而产生细胞内反应
  • 批准号:
    07458205
  • 财政年份:
    1995
  • 资助金额:
    $ 3.97万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Establishment of stable cells by induction of cDNAs of functional proteins and preparation of models for evaluation of drug efficacy for creation of new drugs
通过功能蛋白cDNA诱导建立稳定细胞并制备用于新药研发的药效评价模型
  • 批准号:
    07557195
  • 财政年份:
    1995
  • 资助金额:
    $ 3.97万
  • 项目类别:
    Grant-in-Aid for Scientific Research (A)
Molecular and Cellular Biological Study on the Actions of Intracellular Calcium Ion in Cultured Cells
培养细胞内钙离子作用的分子和细胞生物学研究
  • 批准号:
    05454668
  • 财政年份:
    1993
  • 资助金额:
    $ 3.97万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (B)
Study on long-term potentiation of brain hippocampus
大脑海马长时程增强研究
  • 批准号:
    04044134
  • 财政年份:
    1992
  • 资助金额:
    $ 3.97万
  • 项目类别:
    Grant-in-Aid for international Scientific Research

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Cardiomyocyte CaM kinase II as a driver of cardiac inflammation and remodeling
心肌细胞 CaM 激酶 II 作为心脏炎症和重塑的驱动因素
  • 批准号:
    10308392
  • 财政年份:
    2018
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Targeting CaM Kinase II for Neuroprotection in Ischemic Stroke
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Gating the activation and tuning the Ca2+ frequency response of CaM kinase II
门控 CaM 激酶 II 的激活并调节 Ca2 频率响应
  • 批准号:
    8737282
  • 财政年份:
    2012
  • 资助金额:
    $ 3.97万
  • 项目类别:
Gating the activation and tuning the Ca2+ frequency response of CaM kinase II
门控 CaM 激酶 II 的激活并调节 Ca2 频率响应
  • 批准号:
    8550104
  • 财政年份:
    2012
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Gating the activation and tuning the Ca2+ frequency response of CaM kinase II
门控 CaM 激酶 II 的激活并调节 Ca2 频率响应
  • 批准号:
    8276424
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Developing Ca2+/CaM Kinase II Inhibitors to Treat Arrhythmias in Heart Failure
开发 Ca2/CaM 激酶 II 抑制剂来治疗心力衰竭引起的心律失常
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    8393257
  • 财政年份:
    2012
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Synaptic signaling and remodeling by CaM kinase II
CaM 激酶 II 的突触信号传导和重塑
  • 批准号:
    266034
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    2012
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    Operating Grants
Targeting CaM Kinase II and Oxidative Damage in Allergic Asthma
针对过敏性哮喘中的 CaM 激酶 II 和氧化损伤
  • 批准号:
    8201775
  • 财政年份:
    2011
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PHOSOLAMBAN AND CAM KINASE II IN STOMACH SMOOTH MUSCLE PLASTICITY
福索兰班和 CAM 激酶 II 在胃平滑肌可塑性中的作用
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    8360517
  • 财政年份:
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PHOSOLAMBAN AND CAM KINASE II IN STOMACH SMOOTH MUSCLE PLASTICITY
福索兰班和 CAM 激酶 II 在胃平滑肌可塑性中的作用
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