GRK2 as a novel gene therapy target in heart failure.
暂无分享,去创建一个
[1] W. Koch,et al. Comparative Cardiac Gene Delivery of Adeno‐Associated Virus Serotypes 1–9 reveals that AAV6 Mediates the Most Efficient Transduction in Mouse Heart , 2010, Clinical and translational science.
[2] G. Dorn,et al. Reduction of Sympathetic Activity via Adrenal-targeted GRK2 Gene Deletion Attenuates Heart Failure Progression and Improves Cardiac Function after Myocardial Infarction* , 2010, The Journal of Biological Chemistry.
[3] D. Leosco,et al. Adrenal GRK2 lowering is an underlying mechanism for the beneficial sympathetic effects of exercise training in heart failure. , 2010, American journal of physiology. Heart and circulatory physiology.
[4] W. Koch,et al. Dynamic Changes in Lymphocyte GRK2 Levels in Cardiac Transplant Patients: A Biomarker for Left Ventricular Function , 2010, Clinical and translational science.
[5] D. Mancini,et al. Calcium upregulation by percutaneous administration of gene therapy in cardiac disease (CUPID Trial), a first-in-human phase 1/2 clinical trial. , 2009, Journal of cardiac failure.
[6] W. Koch,et al. Myocardial Adeno-Associated Virus Serotype 6–&bgr;ARKct Gene Therapy Improves Cardiac Function and Normalizes the Neurohormonal Axis in Chronic Heart Failure , 2009, Circulation.
[7] David M. Harris,et al. Uncovering G protein-coupled receptor kinase-5 as a histone deacetylase kinase in the nucleus of cardiomyocytes , 2008, Proceedings of the National Academy of Sciences.
[8] S. Houser,et al. G Protein-Coupled Receptor Kinase 2 Ablation in Cardiac Myocytes Before or After Myocardial Infarction Prevents Heart Failure , 2008, Circulation research.
[9] W. Koch,et al. Gene therapy in heart failure. , 2008, Circulation research.
[10] Yoshiaki Kawase,et al. Design of a phase 1/2 trial of intracoronary administration of AAV1/SERCA2a in patients with heart failure. , 2008, Journal of cardiac failure.
[11] J. Rabinowitz,et al. Analysis of AAV serotypes 1-9 mediated gene expression and tropism in mice after systemic injection. , 2008, Molecular therapy : the journal of the American Society of Gene Therapy.
[12] W. Koch,et al. Modulation of adrenal catecholamine secretion by in vivo gene transfer and manipulation of G protein-coupled receptor kinase-2 activity. , 2008, Molecular therapy : the journal of the American Society of Gene Therapy.
[13] W. Koch,et al. Adrenal adrenoceptors in heart failure: fine-tuning cardiac stimulation. , 2007, Trends in molecular medicine.
[14] M. Gao,et al. New signaling pathways associated with increased cardiac adenylyl cyclase 6 expression: implications for possible congestive heart failure therapy. , 2007, Trends in cardiovascular medicine.
[15] A. Remppis,et al. Stable Myocardial-Specific AAV6-S100A1 Gene Therapy Results in Chronic Functional Heart Failure Rescue , 2007, Circulation.
[16] W. Koch,et al. Adrenal GRK2 upregulation mediates sympathetic overdrive in heart failure , 2007, Nature Medicine.
[17] G. Dorn,et al. Cardiac-Specific Ablation of G-Protein Receptor Kinase 2 Redefines Its Roles in Heart Development and &bgr;-Adrenergic Signaling , 2006, Circulation research.
[18] W. Koch,et al. Lymphocyte levels of GRK2 (betaARK1) mirror changes in the LVAD-supported failing human heart: lower GRK2 associated with improved beta-adrenergic signaling after mechanical unloading. , 2006, Journal of cardiac failure.
[19] W. Koch,et al. Acute ischemic cardiac dysfunction is attenuated via gene transfer of a peptide inhibitor of the β‐adrenergic receptor kinase (βARK1) , 2005 .
[20] D. Leosco,et al. Elevated myocardial and lymphocyte GRK2 expression and activity in human heart failure. , 2005, European heart journal.
[21] Andrew N. Carr,et al. Enhancement of Cardiac Function and Suppression of Heart Failure Progression By Inhibition of Protein Phosphatase 1 , 2005, Circulation research.
[22] N. Dalton,et al. Intracoronary Adenovirus Encoding Adenylyl Cyclase VI Increases Left Ventricular Function in Heart Failure , 2004, Circulation.
[23] N. Dzimiri,et al. Differential functional expression of human myocardial G protein receptor kinases in left ventricular cardiac diseases. , 2004, European journal of pharmacology.
[24] W. Koch,et al. Targeted &bgr;-Adrenergic Receptor Kinase (&bgr;ARK1) Inhibition by Gene Transfer in Failing Human Hearts , 2004 .
[25] S. Emani,et al. Right ventricular targeted gene transfer of a beta-adrenergic receptor kinase inhibitor improves ventricular performance after pulmonary artery banding. , 2004, The Journal of thoracic and cardiovascular surgery.
[26] W. Koch,et al. Viral-based myocardial gene therapy approaches to alter cardiac function. , 2004, Annual review of physiology.
[27] W. Koch,et al. Targeted (cid:1) -Adrenergic Receptor Kinase ( (cid:1) ARK1) Inhibition by Gene Transfer in Failing Human Hearts , 2004 .
[28] W. Koch,et al. The β-adrenergic receptor kinase in heart failure , 2003 .
[29] G. Nagy,et al. Differential control of adrenal and sympathetic catecholamine release by alpha 2-adrenoceptor subtypes. , 2003, Molecular endocrinology.
[30] R. Lefkowitz,et al. Inhibition of βARK1 restores impaired biochemical β-adrenergic receptor responsiveness but does not rescue CREBA133 induced cardiomyopathy , 2002 .
[31] A. Gerdes,et al. Myocyte Redistribution of GRK2 and GRK5 in Hypertensive, Heart-Failure–Prone Rats , 2002, Hypertension.
[32] Harvard Medical School,et al. Targeting Phospholamban by Gene Transfer in Human Heart Failure , 2002, Circulation.
[33] M. Caron,et al. Endocytosis of G protein-coupled receptors: roles of G protein-coupled receptor kinases and ß-arrestin proteins , 2002, Progress in Neurobiology.
[34] Robert J. Lefkowitz,et al. Seven-transmembrane-spanning receptors and heart function , 2002, Nature.
[35] R. Lefkowitz,et al. Signalling: Seven-transmembrane receptors , 2002, Nature Reviews Molecular Cell Biology.
[36] S. Emani,et al. Right ventricular gene therapy with a beta-adrenergic receptor kinase inhibitor improves survival after pulmonary artery banding. , 2001, The Annals of thoracic surgery.
[37] W. Koch,et al. Ventricular Dysfunction After Cardioplegic Arrest Is Improved After Myocardial Gene Transfer of a &bgr;-Adrenergic Receptor Kinase Inhibitor , 2001, Circulation.
[38] C. Scorer,et al. Expression of GRK2 is increased in the left ventricles of cardiomyopathic hamsters , 2001, Basic Research in Cardiology.
[39] R. Lefkowitz,et al. Cardiac βARK1 inhibition prolongs survival and augments β blocker therapy in a mouse model of severe heart failure , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[40] L. Leinwand,et al. Alterations in cardiac adrenergic signaling and calcium cycling differentially affect the progression of cardiomyopathy. , 2001, The Journal of clinical investigation.
[41] S. Emani,et al. In Vivo Ventricular Gene Delivery of a &bgr;-Adrenergic Receptor Kinase Inhibitor to the Failing Heart Reverses Cardiac Dysfunction , 2001, Circulation.
[42] B. Kobilka,et al. Dual modulation of cell survival and cell death by beta(2)-adrenergic signaling in adult mouse cardiac myocytes. , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[43] C. Dellorusso,et al. In vivo acceleration of heart relaxation performance by parvalbumin gene delivery. , 2001, The Journal of clinical investigation.
[44] E. Lakatta,et al. The β2-Adrenergic receptor delivers an antiapoptotic signal to cardiac myocytes through Gi-Dependent coupling to phosphatidylinositol 3'-kinase , 2000 .
[45] R. Lefkowitz,et al. Preservation of myocardial β-adrenergic receptor signaling delays the development of heart failure after myocardial infarction , 2000 .
[46] M. Bristow. β-Adrenergic Receptor Blockade in Chronic Heart Failure , 2000 .
[47] Catherine Communal,et al. Opposing Effects of β1- and β2-Adrenergic Receptors on Cardiac Myocyte Apoptosis Role of a Pertussis Toxin–Sensitive G Protein , 1999 .
[48] K. Propert,et al. Immune responses to adenovirus and adeno-associated virus in humans , 1999, Gene Therapy.
[49] R. Lefkowitz,et al. In Vivo Inhibition of Elevated Myocardial β-Adrenergic Receptor Kinase Activity in Hybrid Transgenic Mice Restores Normal β-Adrenergic Signaling and Function , 1999 .
[50] G. Dorn,et al. Low- and high-level transgenic expression of β2-adrenergic receptors differentially affect cardiac hypertrophy and function in Gαq-overexpressing mice , 1999 .
[51] R. Lefkowitz,et al. Reciprocal in vivo regulation of myocardial G protein-coupled receptor kinase expression by beta-adrenergic receptor stimulation and blockade. , 1998, Circulation.
[52] Marc G. Caron,et al. Control of Myocardial Contractile Function by the Level of β-Adrenergic Receptor Kinase 1 in Gene-targeted Mice* , 1998, The Journal of Biological Chemistry.
[53] J. Ross,et al. Expression of a beta-adrenergic receptor kinase 1 inhibitor prevents the development of myocardial failure in gene-targeted mice. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[54] R. Lefkowitz,et al. Restoration of beta-adrenergic signaling in failing cardiac ventricular myocytes via adenoviral-mediated gene transfer. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[55] W. Koch,et al. Mechanism of β-Adrenergic Receptor Desensitization in Cardiac Hypertrophy Is Increased β-Adrenergic Receptor Kinase* , 1997, The Journal of Biological Chemistry.
[56] J. Benovic,et al. G-protein-coupled receptor kinase activity is increased in hypertension. , 1997, The Journal of clinical investigation.
[57] M. Drazner,et al. Potentiation of beta-adrenergic signaling by adenoviral-mediated gene transfer in adult rabbit ventricular myocytes. , 1997, The Journal of clinical investigation.
[58] D. Clapham,et al. G PROTEIN BETA GAMMA SUBUNITS , 1997 .
[59] M. Caron,et al. Essential role of beta-adrenergic receptor kinase 1 in cardiac development and function. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[60] R. Lefkowitz,et al. Receptor-specific in vivo desensitization by the G protein-coupled receptor kinase-5 in transgenic mice. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[61] M. Lohse,et al. Activation of β-Adrenergic Receptor Kinase During Myocardial Ischemia , 1996 .
[62] R. Lefkowitz,et al. Cardiac function in mice overexpressing the beta-adrenergic receptor kinase or a beta ARK inhibitor. , 1995, Science.
[63] R. Lefkowitz,et al. Structure and mechanism of the G protein-coupled receptor kinases. , 1993, The Journal of biological chemistry.
[64] M. Packer,et al. The development of positive inotropic agents for chronic heart failure: how have we gone astray? , 1993, Journal of the American College of Cardiology.
[65] M. Böhm,et al. Altered expression of beta-adrenergic receptor kinase and beta 1-adrenergic receptors in the failing human heart. , 1993, Circulation.
[66] M. Lohse,et al. Altered Expression of, ‐Adrenergic Receptor Kinase and 1‐Adrenergic Receptors in the Failing Human Heart , 1993 .
[67] O. Brodde. Beta-adrenoceptors in cardiac disease. , 1993, Pharmacology & therapeutics.
[68] S. Jamieson,et al. Beta 1- and beta 2-adrenergic-receptor subpopulations in nonfailing and failing human ventricular myocardium: coupling of both receptor subtypes to muscle contraction and selective beta 1-receptor down-regulation in heart failure. , 1986, Circulation research.
[69] S. Jamieson,et al. β1‐ and β2‐Adrenergic‐Receptor Subpopulations in Nonfailing and Failing Human Ventricular Myocardium: Coupling of Both Receptor Subtypes to Muscle Contraction and Selective β1‐Receptor Down‐Regulation in Heart Failure , 1986 .
[70] D C Harrison,et al. Decreased catecholamine sensitivity and beta-adrenergic-receptor density in failing human hearts. , 1982, The New England journal of medicine.