| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 10953877 | Journal of Molecular and Cellular Cardiology | 2012 | 13 Pages |
Abstract
⺠We investigate the mechanism(s) by which caveolae compartmentalise β2-AR signalling. ⺠Disrupting caveolae reveals β2-AR cAMP signals in the PKA-RII compartment. ⺠Disrupting caveolae promotes a selective PKA-mediated phosphorylation of PLB. ⺠Phosphatases (PP) 1/2a (but not PDE 2/3/4) contribute to caveolar β2-AR compartmentation. ⺠We propose that intact caveolae attenuate cAMP production and limit inhibitory modulation of PP at the SR.
Keywords
MbCDCGP20712Aerythro-9-(2-hydroxy-3-nonyl)adenineZnTARVMPLBAKAPEHNAbeta adrenoceptorEpacβ-ARforskolinRyRIBMXpKaCGPPDEFsk3-isobutyl-1-methylxanthinecyclic AMPcAMPICa,LL-type Ca2+ currentTnIβ2-AdrenoceptorFluorescence resonance energy transferFRETISOTATtrans-activating transcriptional activatorTroponin ICompartmentationCaveolaePhosphatasePhosphodiesterasephospholambanmethyl-β-cyclodextrinhuman immunodeficiency virusHIVA kinase anchoring proteinprotein phosphatasesexchange protein activated by cAMPprotein kinase ACav-3Caveolin-3Ryanodine receptor
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Authors
David A. MacDougall, Shailesh R. Agarwal, Elizabeth A. Stopford, Hongjin Chu, Jennifer A. Collins, Anna L. Longster, John Colyer, Robert D. Harvey, Sarah Calaghan,