Apoptosis Repressor With Caspase Recruitment Domain Is Required for Cardioprotection in Response to Biomechanical and Ischemic Stress
暂无分享,去创建一个
R. Dietz | V. Gross | S. Donath | Peifeng Li | R. von Harsdorf | T. Willnow | J. Bauersachs | N. Al-Saadi | K. Wollert | M. Bader | U. Martin | C. Willenbockel | N. al-Saadi
[1] Michael D Schneider,et al. Learning from failure: congestive heart failure in the postgenomic age. , 2005, The Journal of clinical investigation.
[2] J. Ross,et al. Small proline‐rich protein 1A is a gp130 pathway‐ and stress‐inducible cardioprotective protein , 2004, The EMBO journal.
[3] S. Akira,et al. Pressure Overload Induces Cardiac Dysfunction and Dilation in Signal Transducer and Activator of Transcription 6-Deficient Mice , 2004, Circulation.
[4] S. Korsmeyer,et al. Inhibition of both the extrinsic and intrinsic death pathways through nonhomotypic death-fold interactions. , 2004, Molecular cell.
[5] Michael D. Schneider,et al. Signal Transducer and Activator of Transcription 3 Is Required for Myocardial Capillary Growth, Control of Interstitial Matrix Deposition, and Heart Protection From Ischemic Injury , 2004, Circulation research.
[6] M. Crow,et al. Apoptosis Repressor with Caspase Recruitment Domain Protects against Cell Death by Interfering with Bax Activation* , 2004, Journal of Biological Chemistry.
[7] P. Poole‐Wilson,et al. Regenerative capacity of the myocardium: implications for treatment of heart failure , 2004, The Lancet.
[8] G. Dorn,et al. Phenotyping hypertrophy: eschew obfuscation. , 2003, Circulation research.
[9] T. Gardner,et al. Blocking the development of postischemic cardiomyopathy with viral gene transfer of the apoptosis repressor with caspase recruitment domain. , 2003, The Journal of thoracic and cardiovascular surgery.
[10] N. Maulik,et al. Bax ablation protects against myocardial ischemia-reperfusion injury in transgenic mice. , 2003, American journal of physiology. Heart and circulatory physiology.
[11] R. Kitsis,et al. A mechanistic role for cardiac myocyte apoptosis in heart failure. , 2003, The Journal of clinical investigation.
[12] S. Vatner,et al. Activation of Mst1 causes dilated cardiomyopathy by stimulating apoptosis without compensatory ventricular myocyte hypertrophy. , 2003, The Journal of clinical investigation.
[13] J. Schaper,et al. Myocytes Die by Multiple Mechanisms in Failing Human Hearts , 2003, Circulation research.
[14] P. Anversa,et al. Myocyte death, growth, and regeneration in cardiac hypertrophy and failure. , 2003, Circulation research.
[15] S. Silver,et al. Heart Failure , 1937, The New England journal of medicine.
[16] Martin Ungerer,et al. Essential myosin light chain as a target for caspase-3 in failing myocardium , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[17] M. Crow,et al. TAT Protein Transduction Into Isolated Perfused Hearts: TAT–Apoptosis Repressor With Caspase Recruitment Domain Is Cardioprotective , 2002, Circulation.
[18] R. Dietz,et al. Phosphorylation by protein kinase CK2: a signaling switch for the caspase-inhibiting protein ARC. , 2002, Molecular cell.
[19] K. Chien,et al. Absence of pressure overload induced myocardial hypertrophy after conditional inactivation of Gαq/Gα11 in cardiomyocytes , 2001, Nature Medicine.
[20] Stephanie Birkey Reffey,et al. Characterization of XIAP-Deficient Mice , 2001, Molecular and Cellular Biology.
[21] K. Chien,et al. Absence of pressure overload induced myocardial hypertrophy after conditional inactivation of Galphaq/Galpha11 in cardiomyocytes. , 2001, Nature medicine.
[22] K. Chien,et al. Stress Pathways and Heart Failure , 1999, Cell.
[23] J. Ross,et al. Loss of a gp130 Cardiac Muscle Cell Survival Pathway Is a Critical Event in the Onset of Heart Failure during Biomechanical Stress , 1999, Cell.
[24] J. Ross,et al. Distinct molecular phenotypes in murine cardiac muscle development, growth, and hypertrophy. , 1998, Journal of molecular and cellular cardiology.
[25] John W. Adams,et al. Enhanced Galphaq signaling: a common pathway mediates cardiac hypertrophy and apoptotic heart failure. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[26] S. Chen,et al. ARC, an inhibitor of apoptosis expressed in skeletal muscle and heart that interacts selectively with caspases. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[27] P. Anversa,et al. Apoptosis and myocardial infarction , 1998, Basic Research in Cardiology.
[28] C A Beltrami,et al. Apoptosis in the failing human heart. , 1997, The New England journal of medicine.
[29] P. Hornsby,et al. Presence of double-strand breaks with single-base 3' overhangs in cells undergoing apoptosis but not necrosis , 1996, The Journal of cell biology.
[30] L. Gaboury,et al. Apoptosis in pressure overload-induced heart hypertrophy in the rat. , 1996, The Journal of clinical investigation.
[31] R. Kloner,et al. Reperfusion injury induces apoptosis in rabbit cardiomyocytes. , 1994, The Journal of clinical investigation.
[32] S. Korsmeyer,et al. Bcl-2-deficient mice demonstrate fulminant lymphoid apoptosis, polycystic kidneys, and hypopigmented hair , 1993, Cell.
[33] J. Ross,et al. Segregation of atrial-specific and inducible expression of an atrial natriuretic factor transgene in an in vivo murine model of cardiac hypertrophy , 1991, Proceedings of the National Academy of Sciences of the United States of America.