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Molecular Anatomy of Gap Junction Expression Regulation Effect in Conditional Cx Knockout Mice

Molecular Anatomy of Gap Junction Expression Regulation Effect in Conditional Cx Knockout Mice
条件性 Cx 基因敲除小鼠间隙连接表达调控效应的分子解剖学
批准号:
13470004
负责人:
SHIBATA Yosaburo
金额:
$9.09万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (B)
财政年份:
2001
资助国家:
日本
项目状态:
已结题
起止时间:
2001 至 2002

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中文摘要
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英文摘要
1. We have created mice whose floxed-Cx45 locus can be removed conditionally. They are healthy when Cre is absent. However, cardiac α-actin-Cre-mediated Cx45-deletion resulted in early embryonic lethality. X-gal staining, a hallmark of Cre/loxP-mediated floxed-Cx45 deletion, was detected in the embryonic cardiac myocytes. In another experiment, embryonic cardiac myocytes were differentiated from Cx45-deficient ES cells in vitro. Their conduction velocity was slow, but contraction rhythm was rapid and irregular. Therefore we, for the first time, found that Cx45 is an essential gap junction protein required for the early embryonic cardiac myocytes.2. On the other hand, smooth muscle α-actin-Cre-mediated Cx45-deletion yielded healthy mice, indicating that Cx45 is not essential in smooth muscle. However, Cx45 is so widely expressed in the smooth muscle cells that its detailed function on vascular smooth muscle remains to be clarified. We are examining how this vascular smooth muscle-specific Cx45 knockout affects the integrity and regulation of vascular tone.3. The attempt to detect Cx43-Cx45 doubly deficient mice by a micro-drop culture system was not successful. At present, the fact seemingly indicates that a significant defect may impair early eggs when both connexins are lost. We are trying to create Cx43-KO/floxed-Cx45 mice, which will enable us to explore Cx43-Cx45 doubly deficient mice/cells in desired cell types at desired timing.4. We have unraveled a detailed spatio-temporal expression profile of the Cx45-marker in the central nervous system. Strong expression in the thalamus was a novel finding. These data make ongoing collaboration very exciting (with Prof. David Paul at Harvard Medical School and Prof. Cecilia Lo at NIH, to create neuron/glia/neural crest-specific knockout of Cx45).
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H.Koga et al.: "Overexpression of Polycomb-group gene rae28 in cardiomyocytes does not complement abnormal cardiac morphogenesis in mice lacking rae28 but causes dilated cardiomyopathy"Lab. Invest.. 82・4. 375-385 (2002)
H. Koga 等人:“心肌细胞中 Polycomb 组基因 rae28 的过度表达不会补充缺乏 rae28 的小鼠的异常心脏形态发生,但会导致扩张型心肌病”Lab. 82・4 (2002)。
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M.Doiguchi et al.: "Spergen-1 might be an adhesive molecule associated with mitochondria in the middle piece of spermatozoa"Dev. Biol.. 252・1. 127-137 (2002)
M.Doiguchi 等人:“Spergen-1 可能是与精子中段线粒体相关的粘附分子”Dev. Biol.. 127-137 (2002)。
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柴田 洋三郎: "ギャップ結合の微細構造と分子生物学"電子顕微鏡. 36. 156-162 (2001)
Yozaburo Shibata:“间隙连接的精细结构和分子生物学”电子显微镜 36. 156-162 (2001)。
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26
    Comparative and molecular anatomical research of GAP junction-related molecules.
    • 批准号:
      19390052
    • 项目类别:
      Grant-in-Aid for Scientific Research (B)
    • 资助金额:
      $12.06万
    • 财政年份:
      2007
    • 负责人:
      SHIBATA Yosaburo
    • 依托单位:
    Molecular anatomical research for the role of gap junction proteins in cardiac function.
    • 批准号:
      17390052
    • 项目类别:
      Grant-in-Aid for Scientific Research (B)
    • 资助金额:
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    • 财政年份:
      2005
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      SHIBATA Yosaburo
    • 依托单位:
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      15390057
    • 项目类别:
      Grant-in-Aid for Scientific Research (B)
    • 资助金额:
      $9.73万
    • 财政年份:
      2003
    • 负责人:
      SHIBATA Yosaburo
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    • 项目类别:
      Grant-in-Aid for Scientific Research (B).
    • 资助金额:
      $8.83万
    • 财政年份:
      1999
    • 负责人:
      SHIBATA Yosaburo
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