Abstract
Caveolae are membrane invaginations that play a critical role in protein trafficking and many signal transduction pathways. Their principal proteins, caveolin-1 (CAV1) and caveolin-2 (CAV2), are highly co-expressed in endothelial cells and pneumocytes. Phenotypes of CAV1 (-/-) and CAV2 (-/-) mice closely resemble pulmonary arterial hypertension (PAH) with CAV2 (-/-) strictly limited to a pulmonary phenotype. It was our hypothesis that genetic variations in CAV2 may contribute to the development of PAH.
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