Dynamics of vesicular tronsformation in maclear complex.
Dynamics of vesicular tronsformation in maclear complex.
批准号:
06557004
负责人:
MARUYAMA Yoshio
金额:
$7.62万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Developmental Scientific Research (B)
财政年份:
1994
资助国家:
日本
项目状态:
已结题
起止时间:
1994 至 1995
中文摘要
胰腺腺泡细胞外核膜为粗面内质网(ER)膜。通过去核收集核膜,将标准的膜片钳技术应用于这些制剂的外膜。在单通道和全电流水平,1)电压和钙激活的大K通道电流,2)一种外向整流K-通道电流,3)一种内向整流氯通道电流。这些通道可能通过调节内质网释放IP_3和/或循环ADP核糖依赖的Ca~(2+)而参与细胞内Ca~(2+)信号传导。在局部膜-膜水平上,这种变化是随机发生的,是离散的开和离步,可以解释为可逆的囊泡形成(膜转化)。阶跃的大小分布符合负指数曲线,表明膜的转变能似乎有一个单一的能量峰。在整个内质网水平上,随着胞膜Ca~(2+)浓度的增加,膜电容增大。这表明囊泡可逆地转化为帽,在囊泡内部和内质网管腔之间有连接。结果提示,内质网腔内钙离子参与囊泡转运。
英文摘要
The outer nuclear membrane of pancreatic acinar cells serves as a rough endoplasmic reticulum (ER) membrane. Collecting nuclear envelopes by enucleation, the standard patch-clamp techniques were applied to the outer membrane of these preparation. At the single channel and whole-current level, 1) voltage and Ca^<2+>-activated large K-channel current, 2) a type of outward-going rectifier K-channel current, 3) a type of inward-going rectifier Cl-channel current, were found. These channels may contribute to cellular Ca^<2+>-signaling through regulating IP_3-and/or cyclic ADP-ribose-dependent Ca^<2+>-release from the ER.Applying a phase-sensitive capacitance measurement to the ER preparation, the time course of the changes in membrane capacitance were monitored. At the local patch-membrane level, the changes occurred at random as discrete on-and off-steps, which can be interpreted as reversible vesicle formation (membrane transformation). The size distribution of the steps were fitted by a negative exponential curve, suggesting the membrane transformation energy seems to have a single energy peak. Increasing the lumenal Ca^<2+>-concentration at the whole-ER level, a rise in the membrane capacitance was found. This indicates that the vesicles are reversibly transformed to caps with a connection between the vesicle interior and the ER lumen. The result suggests the involvement of the ER lumenal Ca^<2+> in the vesicular transport.
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Maruyama, Y.: "Delay in granular fusion evoked by repetitive cytosolic Ca^<2+> spikes in mouse pancreatic acinar cells" Cell Calcium. 16. 419-430 (1994)
Maruyama, Y.:“小鼠胰腺腺泡细胞中重复的胞质 Ca^2 尖峰引起的颗粒融合延迟”细胞钙。
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通讯作者:
丸山芳夫: "膜容量測定法" 日本生理学雑誌. 56. 363-368 (1994)
Yoshio Maruyama:“膜电容测量方法”日本生理学杂志 56. 363-368 (1994)。
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Maruyama, Y.: "Ca^<2+>-activated K^+-channels in the nuclear envelope isolated from single pancreatic acinar cells." Pflugers Archiv. 430. 148-150 (1995)
Maruyama,Y.:“从单个胰腺腺泡细胞中分离出核膜中的 Ca ^ 2 -激活的 K ^ -通道。”
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Shimade,H.: "A sodium coupled neutral aminoacid cotransporter inhibited by the volatile anaesthtic halothane in megakaryocytes." Jap.J.Physiology. 45. 165-176 (1995)
Shimade,H.:“巨核细胞中被挥发性麻醉剂氟烷抑制的钠偶联中性氨基酸协同转运蛋白。”
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通讯作者:
Shimada,H.: "A sodium coupled neutral aminoacid cotransporter inhibited by the volatile anaesthtic halothane in megakaryocytes." Jap.J.Physiology. 45. 165-176 (1995)
Shimada,H.:“巨核细胞中被挥发性麻醉剂氟烷抑制的钠偶联中性氨基酸协同转运蛋白。”
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共 17 条
Ion channel coupling and membrane plasticity in nucleus and mitochondria
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批准号:23590254
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项目类别:Grant-in-Aid for Scientific Research (C)
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财政年份:2011
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负责人:MARUYAMA Yoshio
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依托单位:
Dynamics of vesicle formation controlled by cellular messenger signaling
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依托单位:
Features of granule motion and of vesicular fusion by local cell signaling
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项目类别:Grant-in-Aid for General Scientific Research (B)
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资助金额:$4.22万
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财政年份:1994
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负责人:MARUYAMA Yoshio
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依托单位:
Control of granular fusion by small molecular GTP-binding protein
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财政年份:1992
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负责人:MARUYAMA Yoshio
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依托单位:
Physiological roles of low molecular weight 20KG GTP-binding protein : Effects on secretion in pancreatic acinar cells.
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财政年份:1989
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依托单位:
The electrical transfer properties of basolateral-, luminal-, and gap junctional cell membrane in exocrine gland acinar cells.
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财政年份:1986
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负责人:MARUYAMA Yoshio
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依托单位:
海外基金