Cytochrome C Maintains Mitochondrial Transmembrane Potential and Atp Generation after Outer Mitochondrial Membrane Permeabilization during the Apoptotic Process
暂无分享,去创建一个
Martin Schuler | Oliver von Ahsen | D. Green | D. Newmeyer | M. Schuler | O. von Ahsen | N. Waterhouse | Douglas R. Green | J. Goldstein | Nigel J. Waterhouse | Donald D. Newmeyer | Joshua C. Goldstein
[1] P. Nicotera,et al. Intracellular ATP, a switch in the decision between apoptosis and necrosis. , 1998, Toxicology letters.
[2] Y. Tsujimoto,et al. Intracellular ATP levels determine cell death fate by apoptosis or necrosis. , 1997, Cancer research.
[3] J C Reed,et al. Bax and adenine nucleotide translocator cooperate in the mitochondrial control of apoptosis. , 1998, Science.
[4] T. Mak,et al. Apoptotic Protease Activating Factor 1 (Apaf-1)–Independent Cell Death Suppression by Bcl-2 , 2000, The Journal of experimental medicine.
[5] J. Mazat,et al. Mitochondria Are Excitable Organelles Capable of Generating and Conveying Electrical and Calcium Signals , 1997, Cell.
[6] S. Korsmeyer,et al. BCL-2 family members and the mitochondria in apoptosis. , 1999, Genes & development.
[7] B. Zhivotovsky,et al. Release of adenylate kinase 2 from the mitochondrial intermembrane space during apoptosis , 1999, FEBS letters.
[8] L M Loew,et al. Intracellular fluorescent probe concentrations by confocal microscopy. , 1998, Biophysical journal.
[9] D L Farkas,et al. Simultaneous imaging of cell and mitochondrial membrane potentials. , 1989, Biophysical journal.
[10] V. Mootha,et al. tBID, a membrane-targeted death ligand, oligomerizes BAK to release cytochrome c. , 2000, Genes & development.
[11] Matthew G. Vander Heiden,et al. Bcl-2 proteins: regulators of apoptosis or of mitochondrial homeostasis? , 1999, Nature Cell Biology.
[12] G M Cohen,et al. Apaf-1 oligomerizes into biologically active approximately 700-kDa and inactive approximately 1.4-MDa apoptosome complexes. , 2000, The Journal of biological chemistry.
[13] Xiaodong Wang,et al. Induction of Apoptotic Program in Cell-Free Extracts: Requirement for dATP and Cytochrome c , 1996, Cell.
[14] D. Green,et al. The Release of Cytochrome c from Mitochondria: A Primary Site for Bcl-2 Regulation of Apoptosis , 1997, Science.
[15] M. V. Heiden,et al. Outer mitochondrial membrane permeability can regulate coupled respiration and cell survival. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[16] S. Srinivasula,et al. Cytochrome c and dATP-Dependent Formation of Apaf-1/Caspase-9 Complex Initiates an Apoptotic Protease Cascade , 1997, Cell.
[17] G. Evan,et al. Inhibition of Ced-3/ICE-related Proteases Does Not Prevent Cell Death Induced by Oncogenes, DNA Damage, or the Bcl-2 Homologue Bak , 1997, The Journal of cell biology.
[18] D. Andrews,et al. Bcl-2 and Bax regulate the channel activity of the mitochondrial adenine nucleotide translocator , 2000, Oncogene.
[19] Gerard I. Evan,et al. The coordinate release of cytochrome c during apoptosis is rapid, complete and kinetically invariant , 2000, Nature Cell Biology.
[20] H. Forman,et al. On the virtual existence of superoxide anions in mitochondria: thoughts regarding its role in pathophysiology , 1997, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[21] Gail Walker,et al. Apaf-1 Oligomerizes into Biologically Active ∼700-kDa and Inactive ∼1.4-MDa Apoptosome Complexes* , 2000, The Journal of Biological Chemistry.
[22] X. Liu,et al. An APAF-1·Cytochrome c Multimeric Complex Is a Functional Apoptosome That Activates Procaspase-9* , 1999, The Journal of Biological Chemistry.
[23] G. Kroemer,et al. The Permeability Transition Pore Complex: A Target for Apoptosis Regulation by Caspases and Bcl-2–related Proteins , 1998, The Journal of experimental medicine.
[24] T. Kuwana,et al. The Pro-Apoptotic Proteins, Bid and Bax, Cause a Limited Permeabilization of the Mitochondrial Outer Membrane That Is Enhanced by Cytosol , 1999, The Journal of cell biology.
[25] Christian Renken,et al. Preservation of Mitochondrial Structure and Function after Bid- or Bax-Mediated Cytochrome c Release , 2000, The Journal of cell biology.
[26] M. Crompton,et al. Cyclophilin-D binds strongly to complexes of the voltage-dependent anion channel and the adenine nucleotide translocase to form the permeability transition pore. , 1998, European journal of biochemistry.
[27] T. Yanagida,et al. Electrophysiological Study of a Novel Large Pore Formed by Bax and the Voltage-dependent Anion Channel That Is Permeable to Cytochrome c * , 2000, The Journal of Biological Chemistry.
[28] Robert L Moritz,et al. Identification of DIABLO, a Mammalian Protein that Promotes Apoptosis by Binding to and Antagonizing IAP Proteins , 2000, Cell.
[29] M. V. Heiden,et al. Bcl-xL prevents cell death following growth factor withdrawal by facilitating mitochondrial ATP/ADP exchange. , 1999, Molecular cell.
[30] S. Lowe,et al. Apaf-1 and caspase-9 in p53-dependent apoptosis and tumor inhibition. , 1999, Science.
[31] Eugene M. Johnson,et al. Caspase Inhibition Extends the Commitment to Neuronal Death Beyond Cytochrome c Release to the Point of Mitochondrial Depolarization , 2000, The Journal of cell biology.
[32] D. Green,et al. Mitochondrial cytochrome c release in apoptosis occurs upstream of DEVD‐specific caspase activation and independently of mitochondrial transmembrane depolarization , 1998, The EMBO journal.
[33] L. Blatter,et al. Fluctuations in mitochondrial membrane potential caused by repetitive gating of the permeability transition pore. , 1999, The Biochemical journal.
[34] Xiaodong Wang,et al. Smac, a Mitochondrial Protein that Promotes Cytochrome c–Dependent Caspase Activation by Eliminating IAP Inhibition , 2000, Cell.
[35] Dean P. Jones,et al. Prevention of Apoptosis by Bcl-2: Release of Cytochrome c from Mitochondria Blocked , 1997, Science.
[36] J. Farber,et al. Two mechanisms by which ATP depletion potentiates induction of the mitochondrial permeability transition. , 1997, The American journal of physiology.
[37] S. Srinivasula,et al. Autoactivation of procaspase-9 by Apaf-1-mediated oligomerization. , 1998, Molecular cell.
[38] J. Martinou,et al. The Release of Cytochrome c from Mitochondria during Apoptosis of NGF-deprived Sympathetic Neurons Is a Reversible Event , 1999, The Journal of cell biology.