Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 282, Issue 22, Pages 16631-16643Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M607948200
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Funding
- NHLBI NIH HHS [R01 HL 57665, N01-HV-28186, P01 HL 70295, R01 HL64793, R01 HL 61371] Funding Source: Medline
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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.
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