572 results on '"Force, Thomas"'
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52. Protein kinase cascades in the regulation of cardiac hypertrophy
53. Highlights of the 2003 scientific sessions of the Heart Failure Society of America: Las Vegas, Nevada, September 21 to 24, 2003
54. Activation of the SAPK pathway by the human STE20 homologue germinal centre kinase
55. Renal ischemia/reperfusion and ATP depletion/repletion in LLC-PK1 cells result in phosphorylation of FKHR and FKHRL1
56. RENAL ISCHEMIA/REPERFUSION AND CHEMICAL ANOXIA/DEXTROSE EXPOSURE IN LLC-PK1 CELLS RESULT IN PHOSPHORYLATION OF THE FORKHEAD TRANSCRIPTION FACTORS FKHR AND FKHRL1
57. 69 - Complicações Cardiovasculares dos Agentes de Tratamento do Câncer
58. Regulation of cardiac hypertrophy in vivo by the stress-activated protein kinases/c-Jun NH2-terminal kinases
59. Calcineurin inhibitors and cardiac hypertrophy
60. Cadherin-11 blockade reduces inflammation-driven fibrotic remodeling and improves outcomes after myocardial infarction
61. Targeted disruption of glycogen synthase kinase-3β in cardiomyocytes attenuates cardiac parasympathetic dysfunction in type 1 diabetic Akita mice
62. Ponatinib-induced cardiotoxicity: delineating the signalling mechanisms and potential rescue strategies
63. Role of the Stress-activated Protein Kinases in Endothelin-induced Cardiomyocyte Hypertrophy
64. Rab-GTPase binding effector protein 2 (RABEP2) is a primed substrate for Glycogen Synthase kinase-3 (GSK3)
65. Correction: Analysis of Tyrosine Kinase Inhibitor-Mediated Decline in Contractile Force in Rat Engineered Heart Tissue
66. Inhibition of GSK-3 to induce cardiomyocyte proliferation: a recipe for in situ cardiac regeneration
67. Stretch-activated pathways and left ventricular remodeling
68. 69 - Complicaciones cardiovasculares de los fármacos para el cáncer
69. Abstract 361: Analysis of Cardiotoxic Mechanisms Associated With Tyrosine Kinase Inhibitor Ponatinib
70. Mitogen-activated protein kinase signaling in the heart: angels versus demons in a heart-breaking tale
71. Abstract 41: Cardiomyocyte-specific Conditional Deletion of GSK-3β Leads to Cardiac Dysfunction in a High Fat Diet Induced Obesity Model
72. Abstract 98: Canonical TGF-β1 Signaling in Cardiomyocytes is Essential to Maintain Basal Cardiac Function
73. Activation of the Amino Acid Response Pathway Blunts the Effects of Cardiac Stress
74. A Novel Positron Emission Tomography (PET) Approach to Monitor Cardiac Metabolic Pathway Remodeling in Response to Sunitinib Malate
75. Targeted disruption of glycogen synthase kinase-3β in cardiomyocytes attenuates cardiac parasympathetic dysfunction in type 1 diabetic Akita mice.
76. Inhibition of GSK-3 to induce cardiomyocyte proliferation: a recipe for in situ cardiac regeneration.
77. A pilot phase II Study of digoxin in patients with recurrent prostate cancer as evident by a rising PSA
78. Imatinib Activates Pathological Hypertrophy by Altering Myocyte Calcium Regulation
79. Heart failure: Preventing disease and death worldwide
80. Abstract 280: Cardiac Fibroblast Specific Deletion of Gsk3α Alleviate From Cardiac Dysfunction and Fibrotic Remodeling in Ischemic Heart
81. Abstract 75: Cardiomyocyte-specific Conditional Deletion of GSK-3β Leads to Global Metabolic Defects and Cardiac Dysfunction in a HFD Induced Obesity Model
82. Abstract 69: Cardiomyocyte GSK-3α Signaling Exacerbate Pressure Overload-induced Dilated Cardiomyopathy and Heart Failure
83. Response by Zhou et al to Letter Regarding Article, “Loss of Adult Cardiac Myocyte GSK-3 Leads to Mitotic Catastrophe Resulting in Fatal Dilated Cardiomyopathy”
84. Loss of Adult Cardiac Myocyte GSK-3 Leads to Mitotic Catastrophe Resulting in Fatal Dilated Cardiomyopathy
85. Analysis of Tyrosine Kinase Inhibitor-Mediated Decline in Contractile Force in Rat Engineered Heart Tissue
86. Introducing JACC: Basic to Translational Science
87. Cardio-Oncology
88. Group IVA Cytosolic Phospholipase A2 Regulates the G2-to-M Transition by Modulating the Activity of Tumor Suppressor SIRT2
89. Colaboradores
90. The weakness of a big heart
91. In reply to 'Cardiotoxicity of the cancer therapeutic agent imatinib mesylate'
92. The GSK-3 Family as Therapeutic Target for Myocardial Diseases
93. Cardiac Hypertrophy
94. Heart failure: preventing disease and death worldwide
95. Expert Consensus for Multimodality Imaging Evaluation of Adult Patients during and after Cancer Therapy: A Report from the American Society of Echocardiography and the European Association of Cardiovascular Imaging
96. Cardiomyocyte-Specific Deletion of Gsk3α Mitigates Post–Myocardial Infarction Remodeling, Contractile Dysfunction, and Heart Failure
97. Cardiac Fibroblast Glycogen Synthase Kinase-3β Regulates Ventricular Remodeling and Dysfunction in Ischemic Heart
98. Imatinib Activates Pathological Hypertrophy by Altering Myocyte Calcium Regulation
99. Sorafenib Cardiotoxicity Increases Mortality After Myocardial Infarction
100. Troponin I-Interacting Protein Kinase
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