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Knockout of cav-1 protein causes loss of a cellular organelle

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By targeted disruption of caveolin-1, the main protein component of caveolae, Drs. Teymuras V. Kurzchalia and Marek Drab and their colleagues have generated mice that lack caveolae. The absence of this organelle impaired nitric oxide and calcium signaling in the cardiovascular system causing aberrations in endothelium-dependent relaxation, contractility, and maintenance of myogenic tone. In addition, the lungs of mutant animals displayed dramatic thickening of alveolar septa caused by uncontrolled endothelial cell proliferation and fibrosis. These defects resulted in severe physical limitations in caveolin-1-disrupted mice but were not lethal. These data demonstrate a fundamental role of caveolin-1 and caveolae in organizing multiple signalling pathways in the cell and indicate important physiological roles for caveolae in lung function and the cardiovascular system.


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Contact: Claudia Lorenz
claudia.lorenz@mpi-cbg.de
49-351-210-2030
Max-Planck-Gesellschaft
10-Aug-2001


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