Published online before print October 27, 2005, doi: 10.1161/01.RES.0000193597.65217.00
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Submitted on September 7, 2005
Revised on October 12, 2005
Accepted on October 18, 2005
Activation of the Endothelial Store-Operated ISOC Ca2+ Channel Requires Interaction of Protein 4.1 With TRPC4
Donna L. Cioffi ;
From the Center for Lung Biology (D.L.C., S.W., T.S.), Department of Pharmacology (D.L.C., S.W., M.A., T.S.), and Department of Cell Biology and Neuroscience (M.A.), the University of South Alabama College of Medicine, Mobile; Department of Molecular and Cell Biology (S.R.G.), the University of Texas at Dallas; and Department of Neuroscience and Center for Molecular Neurobiology (M.X.Z.)5, the Ohio State University, Columbus.
* To whom correspondence should be addressed. E-mail: tstevens{at}jaguar1.usouthal.edu.
Store-operated calcium (SOC) entry represents the principal Ca2+ entry pathway into nonexcitable cells. Despite intensive investigation, mechanisms underlying activation of SOC entry have remained elusive. The endothelial ISOC channel is a Ca2+-selective SOC entry channel to which the transient receptor potential (TRP) proteins TRPC1 and TRPC4 contribute subunits. Activation of ISOC is specifically regulated by the spectrin-actin membrane skeleton; however, the nature of coupling between the ISOC channel and membrane skeleton is unknown. Here we demonstrate that protein 4.1 is an essential component of the ISOC channel-gating mechanism. Protein 4.1 interacts with TRPC4 and the membrane skeleton. Deletion of the protein 4.1 binding domain on TRPC4 or peptide competition to the protein 4.1 binding domain prevents ISOC activation. These findings reveal that interaction of protein 4.1 with TRPC4 is required for activation of the endothelial ISOC channel.
Key words: cytoskeleton • ISOC • spectrin • store-operated Ca2+ • entry • TRPC
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