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CELL ADHESION MOLECULES IN CARDIOGENESIS

CELL ADHESION MOLECULES IN CARDIOGENESIS
心肌发生中的细胞粘附分子
批准号:
2609251
负责人:
MICHIKO WATANABE
金额:
$18.47万
依托单位国家:
美国
项目类别:
财政年份:
1988
资助国家:
美国
项目状态:
已结题
起止时间:
1988-07-01 至 2000-11-30

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中文摘要
翻译
描述(摘自申请者摘要):聚唾液酸的作用 NCAM在心脏传导系统的正常发育中会 在鸡胚模型中进行了研究。神经细胞黏附 NCAM分子及其聚唾液酸部分是细胞-细胞间的调节剂 在发育中的心脏中发现相互作用。向上和向下调节 神经和骨骼肌发育过程中的这些成分是 对于创造导致正常形态发生的平衡至关重要 模式。在以前的研究中,申请人已经证明了NCAM 和PSA在发育中的心脏组织中的表达受到调控。 她还表明,NCAM或PSA的扰动会改变功能 连接心肌细胞和富含PSA的NCAM的缝隙连接是 多见于脑室传导组织。这些发现 导致调查人员建议NCAM和PSA充当他们的角色 DO在神经元突起的相互作用中允许可塑性 心肌细胞,特别是传导组织的心肌细胞 心脏生成。本研究的目的是:1)完善这一假说 通过确定PSA在区域和阶段中的分布 详细研究;和2)通过酶学方法检验他们的假设 从受精卵胚胎心脏中去除PSA并评估 对细胞形态、生化和电生理的影响 传导系统。
英文摘要
DESCRIPTION (taken from applicants abstract): The role of polysialated NCAM in the normal development of the cardiac conduction system will be investigated in the chicken embryo model. The neural cell adhesion molecule NCAM and its polysialic acid moiety are modulators of cell-cell interactions found in the developing heart. Up and down regulation of these components during neural and skeletal muscle development is critical for creating the balance that results in normal morphogenetic patterns. In previous studies, the applicant has demonstrated that NCAM and PSA are regulated in their expression in developing heart tissue. She has also shown that perturbation of NCAM or PSA alters the function of gap junctions which couple myocardial cells and PSA-rich NCAM is found preferentially on ventricular conduction tissue. These findings has led the investigator to propose that NCAM and PSA are acting as they do on neuronal processes to allow plasticity in interactions of myocardial cells, particularly those of conduction tissue during cardiogenesis. The aims of this study are: 1) to refine this hypothesis by determining the PSA distribution in regions and stages not yet studied in detail; and 2) to test their hypothesis by enzymatically removing PSA from the embryonic heart in ovo and assessing the consequences to the morphology, biochemistry and electrophysiology of the conduction system.
期刊论文(7)
专著(0)
科研奖励(0)
会议论文
Forced expression of the homeodomain protein Gax inhibits cardiomyocyte proliferation and perturbs heart morphogenesis.
同源结构域蛋白 Gax 的强制表达会抑制心肌细胞增殖并扰乱心脏形态发生。
DOI: 10.1242/dev.124.21.4405
发表时间: 1997
期刊: Development (Cambridge, England)
影响因子: --
作者: [Fisher,SA, Siwik,E, Branellec,D, Walsh,K, Watanabe,M]
通讯作者: Watanabe,M
Expression of exogenous protein and analysis of morphogenesis in the developing chicken heart using an adenoviral vector.
使用腺病毒载体表达外源蛋白并分析发育中鸡心脏的形态发生。
DOI: --
发表时间: 1996
期刊: Cardiovascular research.
影响因子: --
作者: [Fisher,SA, Watanabe,M]
通讯作者: Watanabe,M
Developmental transitions in cardiac conduction.
心脏传导的发育转变。
DOI: --
发表时间: 2003
期刊: Novartis Foundation symposium
影响因子: --
作者: [Watanabe,Michiko, Chuck,EmilThomas, Rothenberg,Florence, Rosenbaum,DavidS]
通讯作者: Rosenbaum,DavidS
Regulation of coronary vascular development by differential tissue hypoxia
  • 批准号:
    7527668
  • 项目类别:
  • 资助金额:
    $51.89万
  • 财政年份:
    2009
  • 负责人:
    MICHIKO WATANABE
  • 依托单位:
Regulation of coronary vascular development by differential tissue hypoxia
  • 批准号:
    7915293
  • 项目类别:
  • 资助金额:
    $47.83万
  • 财政年份:
    2009
  • 负责人:
    MICHIKO WATANABE
  • 依托单位:
The toxin and hypoxia pathways in cardiogenesis
  • 批准号:
    7121217
  • 项目类别:
  • 资助金额:
    $17.04万
  • 财政年份:
    2005
  • 负责人:
    MICHIKO WATANABE
  • 依托单位:
The toxin and hypoxia pathways in cardiogenesis
  • 批准号:
    6855234
  • 项目类别:
  • 资助金额:
    $22.75万
  • 财政年份:
    2005
  • 负责人:
    MICHIKO WATANABE
  • 依托单位:
海外基金