Bcl-2 Is a Key Factor for Cardiac Fibroblast Resistance to Programmed Cell Death
Open Access
- 1 August 2004
- journal article
- Published by Elsevier in Journal of Biological Chemistry
- Vol. 279 (33), 34882-34889
- https://doi.org/10.1074/jbc.m404616200
Abstract
No abstract availableKeywords
This publication has 46 references indexed in Scilit:
- Molecular mechanisms of non-apoptosis by Fas stimulation alone versus apoptosis with an additional actinomycin D in cultured cardiomyocytesCardiovascular Research, 2002
- Fas receptor signaling inhibits glycogen synthase kinase 3β and induces cardiac hypertrophy following pressure overloadJournal of Clinical Investigation, 2002
- Apoptotic pathway activation from mitochondria and death receptors without caspase-3 cleavage in failing human myocardiumJournal of the American College of Cardiology, 2002
- Myocyte renewal and ventricular remodellingNature, 2002
- Opening of the Mitochondrial Permeability Transition Pore Causes Depletion of Mitochondrial and Cytosolic NAD+and Is a Causative Event in the Death of Myocytes in Postischemic Reperfusion of the HeartJournal of Biological Chemistry, 2001
- Proinflammatory consequences of transgenic Fas ligand expression in the heartJournal of Clinical Investigation, 2000
- Programmed cell death in the developing heartCardiovascular Research, 2000
- Apoptosis in heart failure: Release of cytochrome c from mitochondria and activation of caspase-3 in human cardiomyopathyProceedings of the National Academy of Sciences, 1999
- Changes in E2F Complexes Containing Retinoblastoma Protein Family Members and Increased Cyclin-dependent Kinase Inhibitor Activities During Terminal Differentiation of CardiomyocytesJournal of Molecular and Cellular Cardiology, 1998
- Differential and Dramatic Changes of Cyclin-dependent Kinase Activities in Cardiomyocytes During the Neonatal PeriodJournal of Molecular and Cellular Cardiology, 1997