Inhibition of receptor-localized PI3K preserves cardiac β-adrenergic receptor function and ameliorates pressure overload heart failure

Jeffrey J. Nienaber, Hideo Tachibana, Sathyamangla V. Naga Prasad, Giovanni Esposito, Dianqing Wu, Lan Mao, Howard A. Rockman
2003 Journal of Clinical Investigation  
Jeffrey J. Nienaber and Hideo Tachibana contributed equally to this work. Conflict of interest: The authors have declared that no conflict of interest exists. Nonstandard abbreviations used: β-adrenergic receptor (βAR); G protein-coupled receptors (GPCRs); phosphatidylinositol (PtdIns); phosphoinositide kinase domain (PIK); phosphatidylinositol-3,4,5-tri-phosphate (PtdIns-3,4,5-P3); inactive mutant of PI3Kγ (PI3Kγinact); PI3Kγ knockout (PI3Kγ-KO); hemagglutinin (HA); transverse aortic
more » ... se aortic constriction (TAC); left ventricle (LV); PtdIns-3,4,5-tri-phosphate (PIP3); phosphoprotein kinase B (pPKB); phospho-glycogen synthase kinase (pGSK); extracellular signal-regulated kinase (ERK); LV weight/body weight (LVW/BW); isoproterenol (ISO); immunoblotting (IB); c-terminal region of β-adrenergic receptor kinase-1 (βARK1-ct).
doi:10.1172/jci200318213 fatcat:7xcnubr5w5hmjdg2pxhzfhqqbi