Targeted deletion of apoptosis signal-regulating kinase 1 attenuates left ventricular remodeling
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M. Hori | M. Taniike | K. Otsu | S. Hikoso | H. Nakayama | K. Nishida | H. Ichijo | Y. Higuchi | Y. Matsumura | O. Yamaguchi | S. Kurihara | T. Takeda | Tetsuya Watanabe | M. Asahi | K. Hongo | K. Kashiwase | Y. Kusakari | S. Hirotani | I. Tsujimoto | Toshihiro Takeda
[1] S. Solomon,et al. The decreasing incidence of left ventricular remodeling following myocardial infarction , 1997, Basic Research in Cardiology.
[2] K. Mani,et al. Myocyte apoptosis: programming ventricular remodeling. , 2003, Journal of the American College of Cardiology.
[3] M. Hori,et al. The antioxidant N-2-mercaptopropionyl glycine attenuates left ventricular hypertrophy in in vivo murine pressure-overload model. , 2002, Journal of the American College of Cardiology.
[4] Yasushi Matsumura,et al. Involvement of Nuclear Factor-&kgr;B and Apoptosis Signal-Regulating Kinase 1 in G-Protein–Coupled Receptor Agonist–Induced Cardiomyocyte Hypertrophy , 2002, Circulation.
[5] T Takahashi,et al. ASK1 is required for sustained activations of JNK/p38 MAP kinases and apoptosis , 2001, EMBO reports.
[6] H. Ichijo,et al. Execution of Apoptosis Signal-regulating Kinase 1 (ASK1)-induced Apoptosis by the Mitochondria-dependent Caspase Activation* , 2000, The Journal of Biological Chemistry.
[7] R. Willenheimer. Left ventricular remodelling and dysfunction. Can the process be prevented? , 2000, International journal of cardiology.
[8] L. Rubin,et al. Role of Apoptosis Signal-Regulating Kinase in Regulation of the c-Jun N-Terminal Kinase Pathway and Apoptosis in Sympathetic Neurons , 2000, Molecular and Cellular Biology.
[9] Kazuhito Yamamoto,et al. BCL-2 Is Phosphorylated and Inactivated by an ASK1/Jun N-Terminal Protein Kinase Pathway Normally Activated at G2/M , 1999, Molecular and Cellular Biology.
[10] 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.
[11] P. Rakic,et al. The Jnk1 and Jnk2 Protein Kinases Are Required for Regional Specific Apoptosis during Early Brain Development , 1999, Neuron.
[12] A. Coats,et al. Left ventricular remodelling: common process in patients with different primary myocardial disorders. , 1999, International journal of cardiology.
[13] S. Izumo,et al. Apoptosis: basic mechanisms and implications for cardiovascular disease. , 1998, Circulation research.
[14] R. Patten,et al. Ventricular remodeling and its prevention in the treatment of heart failure. , 1998, Current opinion in cardiology.
[15] Kohei Miyazono,et al. Mammalian thioredoxin is a direct inhibitor of apoptosis signal‐regulating kinase (ASK) 1 , 1998, The EMBO journal.
[16] Q. Li,et al. Overexpression of insulin-like growth factor-1 in mice protects from myocyte death after infarction, attenuating ventricular dilation, wall stress, and cardiac hypertrophy. , 1997, The Journal of clinical investigation.
[17] R. Kitsis,et al. Myocyte apoptosis during acute myocardial infarction in the mouse localizes to hypoxic regions but occurs independently of p53. , 1997, The Journal of clinical investigation.
[18] Minoru Takagi,et al. Induction of Apoptosis by ASK1, a Mammalian MAPKKK That Activates SAPK/JNK and p38 Signaling Pathways , 1997, Science.
[19] P. Anversa,et al. Acute myocardial infarction in humans is associated with activation of programmed myocyte cell death in the surviving portion of the heart. , 1996, Journal of molecular and cellular cardiology.
[20] John Calvin Reed,et al. Programmed myocyte cell death affects the viable myocardium after infarction in rats. , 1996, Experimental cell research.
[21] L. Gaboury,et al. Apoptosis in pressure overload-induced heart hypertrophy in the rat. , 1996, The Journal of clinical investigation.
[22] 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.