Cyclic GMP/PKG-dependent inhibition of TRPC6 channel activity and expression negatively regulates cardiomyocyte NFAT activation Novel mechanism of cardiac stress modulation by PDE5 inhibition.
暂无分享,去创建一个
D. Kass | G. Tomaselli | G. Hesketh | T. Aiba | N. Koitabashi | E. Takimoto | Manling Zhang | J. Rowell
[1] F. Duprat,et al. Sensing pressure in the cardiovascular system: Gq-coupled mechanoreceptors and TRP channels. , 2010, Journal of molecular and cellular cardiology.
[2] J. Hell,et al. Physical and Functional Interaction Between Calcineurin and the Cardiac L-Type Ca2+ Channel , 2009, Circulation research.
[3] Muzamil M. Z. Noorani,et al. Inhibition of TRPC1/TRPC3 by PKG contributes to NO-mediated vasorelaxation. , 2009, American journal of physiology. Heart and circulatory physiology.
[4] E. Schroder,et al. L-Type Calcium Channel C Terminus Autoregulates Transcription , 2009, Circulation research.
[5] D. Kass,et al. Cyclic GMP signaling in cardiovascular pathophysiology and therapeutics. , 2009, Pharmacology & therapeutics.
[6] H. Ghofrani,et al. A Functional Single-Nucleotide Polymorphism in the TRPC6 Gene Promoter Associated With Idiopathic Pulmonary Arterial Hypertension , 2009, Circulation.
[7] Brian O'Rourke,et al. Electrophysiological Consequences of Dyssynchronous Heart Failure and Its Restoration by Resynchronization Therapy , 2009, Circulation.
[8] D. Kass,et al. Sildenafil stops progressive chamber, cellular, and molecular remodeling and improves calcium handling and function in hearts with pre-existing advanced hypertrophy caused by pressure overload. , 2009, Journal of the American College of Cardiology.
[9] D. Kass,et al. Phosphodiesterase 5 inhibition blocks pressure overload-induced cardiac hypertrophy independent of the calcineurin pathway. , 2008, Cardiovascular research.
[10] D. Kass,et al. Expression, activity, and pro-hypertrophic effects of PDE5A in cardiac myocytes. , 2008, Cellular signalling.
[11] Y. Mori,et al. Nitric oxide–cGMP–protein kinase G pathway negatively regulates vascular transient receptor potential channel TRPC6 , 2008, The Journal of physiology.
[12] J. O-Uchi,et al. Interaction of &agr;1-Adrenoceptor Subtypes With Different G Proteins Induces Opposite Effects on Cardiac L-type Ca2+ Channel , 2008, Circulation research.
[13] H. Brinkmeier,et al. Transient receptor potential cation channels in normal and dystrophic mdx muscle , 2008, Neuromuscular Disorders.
[14] C. Des Rosiers,et al. Sildenafil and cardiomyocyte-specific cGMP signaling prevent cardiomyopathic changes associated with dystrophin deficiency , 2008, Proceedings of the National Academy of Sciences.
[15] David A. Kass,et al. Tackling heart failure in the twenty-first century , 2008, Nature.
[16] D. Kass,et al. Phosphodiesterase type 5: expanding roles in cardiovascular regulation. , 2007, Circulation research.
[17] J. Lowe,et al. Selective Activation of Human Atrial Gα12 and Gα13 by Gαq-coupled Angiotensin and Endothelin Receptors , 2007 .
[18] M. Mongillo,et al. Protein Kinase G Phosphorylates Cav1.2 α1c and β2 Subunits , 2007, Circulation research.
[19] C. Montell,et al. Integration of phosphoinositide- and calmodulin-mediated regulation of TRPC6. , 2007, Molecular cell.
[20] T. O’Connell,et al. Isolation and culture of adult mouse cardiac myocytes. , 2007, Methods in molecular biology.
[21] J. Lowe,et al. Selective activation of human atrial Galpha12 and Galpha13 by Galphaq-coupled angiotensin and endothelin receptors. , 2007, Journal of cardiovascular pharmacology.
[22] J. A. Peters,et al. Transient receptor potential cation channels in disease. , 2007, Physiological reviews.
[23] John McAnally,et al. TRPC6 fulfills a calcineurin signaling circuit during pathologic cardiac remodeling. , 2006, The Journal of clinical investigation.
[24] M. Nishida,et al. TRPC3 and TRPC6 are essential for angiotensin II‐induced cardiac hypertrophy , 2006, The EMBO journal.
[25] E. Olson,et al. Canonical Transient Receptor Potential Channels Promote Cardiomyocyte Hypertrophy through Activation of Calcineurin Signaling* , 2006, Journal of Biological Chemistry.
[26] Y. Hara,et al. TRP Channels: Molecular Diversity and Physiological Function , 2006, Microcirculation.
[27] D. Castrillon,et al. Foxo Transcription Factors Blunt Cardiac Hypertrophy by Inhibiting Calcineurin Signaling , 2006, Circulation.
[28] H. Nakayama,et al. Calcineurin‐dependent cardiomyopathy is activated by TRPC in the adult mouse heart , 2006, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[29] M. Nishida,et al. Transient Receptor Potential Channels in Cardiovascular Function and Disease , 2006, Circulation research.
[30] M. Pericak-Vance,et al. A Mutation in the TRPC6 Cation Channel Causes Familial Focal Segmental Glomerulosclerosis , 2005, Science.
[31] Bernd Zetsche,et al. Local Atrial Natriuretic Peptide Signaling Prevents Hypertensive Cardiac Hypertrophy in Endothelial Nitric-oxide Synthase-deficient Mice* , 2005, Journal of Biological Chemistry.
[32] N. Koitabashi,et al. Carvedilol effectively blocks oxidative stress-mediated downregulation of sarcoplasmic reticulum Ca2+-ATPase 2 gene transcription through modification of Sp1 binding. , 2005, Biochemical and biophysical research communications.
[33] D. Kass,et al. Chronic inhibition of cyclic GMP phosphodiesterase 5A prevents and reverses cardiac hypertrophy , 2005, Nature Medicine.
[34] Da-Zhi Wang,et al. Atrogin-1/muscle atrophy F-box inhibits calcineurin-dependent cardiac hypertrophy by participating in an SCF ubiquitin ligase complex. , 2004, The Journal of clinical investigation.
[35] H. Kwan,et al. Regulation of canonical transient receptor potential isoform 3 (TRPC3) channel by protein kinase G. , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[36] Lin Chen,et al. Transcriptional regulation by calcium, calcineurin, and NFAT. , 2003, Genes & development.
[37] H. Drexler,et al. Inhibition of calcineurin-NFAT hypertrophy signaling by cGMP-dependent protein kinase type I in cardiac myocytes , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[38] R. Weiss,et al. Targeted Inhibition of Calcineurin in Pressure-overload Cardiac Hypertrophy , 2002, The Journal of Biological Chemistry.
[39] J. Molkentin,et al. Impaired cardiac hypertrophic response in Calcineurin Aβ-deficient mice , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[40] Y. Hara,et al. The Transient Receptor Potential Protein Homologue TRP6 Is the Essential Component of Vascular &agr;1-Adrenoceptor–Activated Ca2+-Permeable Cation Channel , 2001, Circulation research.
[41] M. S. Taylor,et al. Highly specific, membrane-permeant peptide blockers of cGMP-dependent protein kinase Ialpha inhibit NO-induced cerebral dilation. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[42] C. Pignier,et al. Characterization of nifedipine-resistant calcium current in neonatal rat ventricular cardiomyocytes. , 2000, American journal of physiology. Heart and circulatory physiology.
[43] A. Fukamizu,et al. Expression and characterization of mouse angiotensin II type 1a receptor tagging hemagglutinin epitope in cultured cells. , 1999, International journal of molecular medicine.
[44] T. Gudermann,et al. Direct activation of human TRPC6 and TRPC3 channels by diacylglycerol , 1999, Nature.
[45] Jeffrey Robbins,et al. A Calcineurin-Dependent Transcriptional Pathway for Cardiac Hypertrophy , 1998, Cell.
[46] N. Takahashi,et al. Nitric oxide, atrial natriuretic peptide, and cyclic GMP inhibit the growth-promoting effects of norepinephrine in cardiac myocytes and fibroblasts. , 1998, The Journal of clinical investigation.
[47] D. Glass,et al. Phosphorylation by cyclic GMP-dependent protein kinase of a synthetic peptide corresponding to the autophosphorylation site in the enzyme. , 1983, The Journal of biological chemistry.