RACK1 binds to inositol 1,4,5-trisphosphate receptors and mediates Ca2+ release
Abstract
RACK1 is not a G protein but closely resembles the heterotrimeric Gβ-subunit. RACK1 serves as a scaffold, linking protein kinase C to its substrates. We demonstrate that RACK1 physiologically binds inositol 1,4,5-trisphosphate receptors and regulates Ca2+ release by enhancing inositol 1,4,5-trisphosphate receptor binding affinity for inositol 1,4,5-trisphosphate. Overexpression of RACK1 or depletion of RACK1 by interference RNA markedly augments or diminishes Ca2+ release, respectively, without affecting Ca2+ entry. These findings establish RACK1 as a physiologic mediator of agonist-induced Ca2+ release.
- Publication:
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Proceedings of the National Academy of Science
- Pub Date:
- February 2004
- DOI:
- 10.1073/pnas.0308567100
- Bibcode:
- 2004PNAS..101.2328P
- Keywords:
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- CELL BIOLOGY