MODELS FOR GENETIC DISORDERS OF CALCIUM TRANSPORT

钙转运遗传疾病模型

基本信息

  • 批准号:
    6343645
  • 负责人:
  • 金额:
    $ 43.55万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    1999
  • 资助国家:
    美国
  • 起止时间:
    1999-01-01 至 2003-12-31
  • 项目状态:
    已结题

项目摘要

The long-term objective of this proposal is to develop a detailed understanding of the role of specific Ca/2+ pumps in cardiovascular and pulmonary physiology in vivo. The Ca/2+-transporting ATPases being studied are the sarco(endo)plasmic reticulum Ca/2+-ATPases (SERCAs), which sequester Ca/2+ in intracellular storage organelles, and the plasma membrane Ca/2+-ATPases (PMCAs), which extrude Ca/2+ from the cell. It is clear that SERCAs and PMCAs serve as effector molecules controlling critical aspects of Ca/2+ homeostasis and signaling, and excitation- contraction coupling in muscle; however, the specific roles of individual isoforms are poorly understood. To obtain this information we are developing mouse models with mutations in each of the Ca/2+ pumps. We have prepared mice with SERCA2, SERCA3, and PMCA2 null mutations, and have demonstrated defective cardiac function in SERCA2 heterozygous mutants and defective endothelium and epithelium dependent relaxation of vascular and pulmonary smooth muscle in SERCA3 null mutants. In aim 1 we will develop mice with null mutations in the PMCA1 and PMCA4 genes, and will also develop a mouse with a modified PMCA1 gene that will produce only the ubiquitous PMCA1b variant, and not the variants with an acidic calmodulin binding domain that are restricted to excitable tissues. These experiments will test the general hypotheses that individual Ca/2+ pumps serve essential housekeeping on organ-specific functions, and may reveal unexpected phenotypes that yield insights regarding the specific functions of these pumps. In aim 2 we will analyze the developmental and histopathological consequences of mutations in each of the Ca/2+ pumps, and will perform studies using both the intact animal and isolated tissues to assess the physiological role of these pumps in cardiovascular and pulmonary tissues. These experiments will test the hypotheses that SERCA and PMCA pumps regulate cardiac contractility and pulmonary and vascular smooth muscle tone and contractility, which in turn affects cardiac function, airway resistance, and arterial blood pressure. We anticipate that the six mutant mouse lives developed in this proposal will become valuable models for analysis of the mechanisms by which Ca/2+-transporting ATPases modulate physiological functions of cardiovascular, pulmonary, and other tissues.
本建议的长期目标是制定详细的

项目成果

期刊论文数量(0)
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GARY EDWARD SHULL其他文献

GARY EDWARD SHULL的其他文献

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{{ truncateString('GARY EDWARD SHULL', 18)}}的其他基金

MODELS FOR GENETIC DISORDERS OF CALCIUM TRANSPORT
钙转运遗传疾病模型
  • 批准号:
    2767612
  • 财政年份:
    1999
  • 资助金额:
    $ 43.55万
  • 项目类别:
RENAL SODIUM TRANSPORTERS IN CONTROL OF ARTERIAL BLOOD PRESSURE
肾钠转运蛋白控制动脉血压
  • 批准号:
    6202277
  • 财政年份:
    1999
  • 资助金额:
    $ 43.55万
  • 项目类别:
MODELS FOR GENETIC DISORDERS OF CALCIUM TRANSPORT
钙转运遗传疾病模型
  • 批准号:
    6139315
  • 财政年份:
    1999
  • 资助金额:
    $ 43.55万
  • 项目类别:
Models of Ion Transport Defects in Heart and Lung
心肺离子传输缺陷模型
  • 批准号:
    7172635
  • 财政年份:
    1999
  • 资助金额:
    $ 43.55万
  • 项目类别:
MODELS FOR GENETIC DISORDERS OF CALCIUM TRANSPORT
钙转运遗传疾病模型
  • 批准号:
    6490635
  • 财政年份:
    1999
  • 资助金额:
    $ 43.55万
  • 项目类别:
Models of Ion Transport Defects in Heart and Lung
心肺离子传输缺陷模型
  • 批准号:
    6730771
  • 财政年份:
    1999
  • 资助金额:
    $ 43.55万
  • 项目类别:
Models of Ion Transport Defects in Heart and Lung
心肺离子传输缺陷模型
  • 批准号:
    6992731
  • 财政年份:
    1999
  • 资助金额:
    $ 43.55万
  • 项目类别:
Models of Ion Transport Defects in Heart and Lung
心肺离子传输缺陷模型
  • 批准号:
    6835193
  • 财政年份:
    1999
  • 资助金额:
    $ 43.55万
  • 项目类别:
MODELS FOR GENETIC DISORDERS OF CALCIUM TRANSPORT
钙转运遗传疾病模型
  • 批准号:
    6627483
  • 财政年份:
    1999
  • 资助金额:
    $ 43.55万
  • 项目类别:
Mouse Models for Ion Homeostasis Defects in Heart
心脏离子稳态缺陷的小鼠模型
  • 批准号:
    7737203
  • 财政年份:
    1999
  • 资助金额:
    $ 43.55万
  • 项目类别:

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