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J. Biol. Chem., Vol. 282, Issue 22, 16631-16643, June 1, 2007
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1
From the
Department of Pharmacology and Program in Vascular Cell Signaling and Therapeutics, Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, Connecticut 06536 and the Department of Pathology, Dartmouth Medical School, Lebanon, New Hampshire 03756
Various cellular signals initiate calcium entry into cells, and there is evidence that lipid rafts and caveolae may concentrate proteins that regulate transmembrane calcium fluxes. Here, using mice deficient in caveolin-1 (Cav-1) and Cav-1 knock-out reconstituted with endothelium-specific Cav-1, we show that Cav-1 is essential for calcium entry in endothelial cells and governs the localization and protein-protein interactions between transient receptor channels C4 and C1. Thus, Cav-1 is required for calcium entry in vascular endothelial cells and perhaps other specialized cell types containing caveolae.
Received for publication, August 18, 2006 , and in revised form, April 4, 2007.
* This work was supported in part by National Institutes of Health Grants R01 HL64793, RO1 HL 61371, R01 HL 57665, and PO1 HL 70295 and NHLBI Contract N01-HV-28186 (Yale Proteomics Contract) from the National Institutes of Health (to W. C. S.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 To whom correspondence should be addressed. E-mail: william.sessa{at}yale.edu.
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