A tale of two mitochondrial channels, MAC and PTP, in apoptosis
暂无分享,去创建一个
[1] S. Korsmeyer,et al. Cell Death Critical Control Points , 2004, Cell.
[2] F. Cecconi,et al. Mitochondrial release of AIF and EndoG requires caspase activation downstream of Bax/Bak‐mediated permeabilization , 2003, The EMBO journal.
[3] A. Halestrap,et al. A pore way to die , 2005 .
[4] K. Kinnally,et al. Is MAC the knife that cuts cytochrome c from mitochondria during apoptosis? , 2006, Cell Death and Differentiation.
[5] B. Antonsson,et al. Activation of calcium‐independent phospholipase A2 (iPLA2) in brain mitochondria and release of apoptogenic factors by BAX and truncated BID , 2005, Journal of neurochemistry.
[6] G. Kroemer,et al. Bcl-2 inhibits the mitochondrial release of an apoptogenic protease , 1996, The Journal of experimental medicine.
[7] A. Halestrap. Mitochondrial permeability: Dual role for the ADP/ATP translocator? , 2004, Nature.
[8] S. Henrickson,et al. Simultaneous multianalyte detection with a nanometer-scale pore. , 2001, Analytical chemistry.
[9] F Gambale,et al. Inhibition of Bax channel-forming activity by Bcl-2. , 1997, Science.
[10] T. Kuwana,et al. Bcl-2-family proteins and the role of mitochondria in apoptosis. , 2003, Current opinion in cell biology.
[11] A. Halestrap. Calcium, mitochondria and reperfusion injury: a pore way to die. , 2006, Biochemical Society transactions.
[12] S. Snyder,et al. Mitochondrial benzodiazepine receptor linked to inner membrane ion channels by nanomolar actions of ligands. , 1993, Proceedings of the National Academy of Sciences of the United States of America.
[13] K. Kinnally,et al. The Role of the Mitochondrial Apoptosis Induced Channel MAC in Cytochrome c Release , 2005, Journal of bioenergetics and biomembranes.
[14] G. Dorn,et al. Cyclophilin D-dependent mitochondrial permeability transition regulates some necrotic but not apoptotic cell death , 2022 .
[15] Ruedi Aebersold,et al. Molecular characterization of mitochondrial apoptosis-inducing factor , 1999, Nature.
[16] S. Korsmeyer,et al. BAX-dependent transport of cytochrome c reconstituted in pure liposomes , 2000, Nature Cell Biology.
[17] M. Zoratti,et al. The mitochondrial permeability transition. , 1995, Biochimica et biophysica acta.
[18] K. Kinnally,et al. Mitochondrial channel activity studied by patch-clamping mitoplasts , 1989, Journal of bioenergetics and biomembranes.
[19] Cristina Muñoz-Pinedo,et al. Different mitochondrial intermembrane space proteins are released during apoptosis in a manner that is coordinately initiated but can vary in duration. , 2006, Proceedings of the National Academy of Sciences of the United States of America.
[20] E. Margoliash,et al. Primary structure of the cytochrome c from the snapping turtle, Chelydra serpentina. , 1966, Biochemistry.
[21] K. Hoyt,et al. Trifluoperazine and dibucaine‐induced inhibition of glutamate‐induced mitochondrial depolarization in rat cultured forebrain neurones , 1997, British journal of pharmacology.
[22] B. Antonsson,et al. Bid, but Not Bax, Regulates VDAC Channels* , 2004, Journal of Biological Chemistry.
[23] S. Korsmeyer,et al. Solution Structure of the Proapoptotic Molecule BID A Structural Basis for Apoptotic Agonists and Antagonists , 1999, Cell.
[24] P. Krammer,et al. Regulation of death receptor-mediated apoptosis pathways. , 2000, The international journal of biochemistry & cell biology.
[25] G. Fiskum,et al. Inhibition of Bax-Induced Cytochrome c Release from Neural Cell and Brain Mitochondria by Dibucaine and Propranolol , 2003, The Journal of Neuroscience.
[26] E. Wang,et al. Bcl-2 potentiates the maximal calcium uptake capacity of neural cell mitochondria. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[27] J C Reed,et al. Dysregulation of apoptosis in cancer. , 1998, The cancer journal from Scientific American.
[28] J. Martinou,et al. Regulation of Bcl-2 proteins and of the permeability of the outer mitochondrial membrane. , 2005, Comptes rendus biologies.
[29] D. Pfeiffer,et al. Cyclosporin A-sensitive and insensitive mechanisms produce the permeability transition in mitochondria. , 1989, Biochemical and biophysical research communications.
[30] K. Franssila,et al. Reduced expression of proapoptotic gene BAX is associated with poor response rates to combination chemotherapy and shorter survival in women with metastatic breast adenocarcinoma. , 1995, Cancer research.
[31] M. Zoratti,et al. Modulation of the mitochondrial megachannel by divalent cations and protons. , 1992, The Journal of biological chemistry.
[32] J. Martinou,et al. Bax Is Present as a High Molecular Weight Oligomer/Complex in the Mitochondrial Membrane of Apoptotic Cells* , 2001, The Journal of Biological Chemistry.
[33] K. Kinnally,et al. Regulation of the mitochondrial apoptosis-induced channel, MAC, by BCL-2 family proteins. , 2006, Biochimica et biophysica acta.
[34] M. V. Vander Heiden,et al. Bcl-x l Promotes the Open Configuration of the Voltage-dependent Anion Channel and Metabolite Passage through the Outer Mitochondrial Membrane* , 2001, The Journal of Biological Chemistry.
[35] R. Kolesnick,et al. Ceramide Channels Increase the Permeability of the Mitochondrial Outer Membrane to Small Proteins* , 2002, The Journal of Biological Chemistry.
[36] J. Martinou,et al. Which came first, the cytochrome c release or the mitochondrial fission? , 2006, Cell Death and Differentiation.
[37] G Waksman,et al. Comparison of the ion channel characteristics of proapoptotic BAX and antiapoptotic BCL-2. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[38] S. Grimm,et al. The permeability transition pore signals apoptosis by directing Bax translocation and multimerization , 2002, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[39] M. Zoratti,et al. Modulation of the mitochondrial permeability transition pore. Effect of protons and divalent cations. , 1992, The Journal of biological chemistry.
[40] Fabio Di Lisa,et al. The mitochondrial permeability transition from in vitro artifact to disease target , 2006, The FEBS journal.
[41] D. Green,et al. The Pathophysiology of Mitochondrial Cell Death , 2004, Science.
[42] Y. Antonenko,et al. Selective effect of inhibitors on inner mitochondrial membrane channels , 1991, FEBS letters.
[43] A. Petros,et al. Solution structure of the antiapoptotic protein bcl-2 , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[44] Guido Kroemer,et al. Mitochondrial control of cell death , 2000, Nature Medicine.
[45] V. Skulachev. Why are mitochondria involved in apoptosis? Permeability transition pores and apoptosis as selective mechanisms to eliminate superoxide‐producing mitochondria and cell , 1996, FEBS letters.
[46] S. Korsmeyer,et al. VDAC2 Inhibits BAK Activation and Mitochondrial Apoptosis , 2003, Science.
[47] Y. Hsu,et al. Conformation of the Bax C‐terminus regulates subcellular location and cell death , 1999, The EMBO journal.
[48] J. Martinou,et al. Bax oligomerization is required for channel-forming activity in liposomes and to trigger cytochrome c release from mitochondria. , 2000, The Biochemical journal.
[49] Guido Kroemer,et al. Mitochondrio‐nuclear translocation of AIF in apoptosis and necrosis , 2000, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[50] M. Knaapen,et al. The role of apoptosis in vascular disease , 2000, The Journal of pathology.
[51] Junying Yuan,et al. Cleavage of BID by Caspase 8 Mediates the Mitochondrial Damage in the Fas Pathway of Apoptosis , 1998, Cell.
[52] M. Prevost,et al. Mitochondrial Release of Caspase-2 and -9 during the Apoptotic Process , 1999, The Journal of experimental medicine.
[53] Jianjie Ma,et al. Mitochondrial Depolarization Accompanies Cytochrome cRelease During Apoptosis in PC6 Cells* , 1999, The Journal of Biological Chemistry.
[54] M. Colombini,et al. VDAC channels mediate and gate the flow of ATP: implications for the regulation of mitochondrial function. , 1997, Biophysical journal.
[55] S. Korsmeyer,et al. Oligomeric Bax is a component of the putative cytochrome c release channel MAC, mitochondrial apoptosis-induced channel. , 2005, Molecular biology of the cell.
[56] Jean-Claude Martinou,et al. Bid-induced Conformational Change of Bax Is Responsible for Mitochondrial Cytochrome c Release during Apoptosis , 1999, The Journal of cell biology.
[57] M. Zoratti,et al. The inner mitochondrial membrane contains ion‐conducting channels similar to those found in bacteria , 1989, FEBS letters.
[58] B. Hille. Ionic channels of excitable membranes , 2001 .
[59] M. Venkatachalam,et al. Bcl-2 Prevents Bax Oligomerization in the Mitochondrial Outer Membrane* , 2001, The Journal of Biological Chemistry.
[60] K. Kinnally,et al. Some amphiphilic cations block the mitochondrial apoptosis‐induced channel, MAC , 2004, FEBS letters.
[61] Seamus J. Martin,et al. Apoptosis‐associated release of Smac/DIABLO from mitochondria requires active caspases and is blocked by Bcl‐2 , 2001, The EMBO journal.
[62] Y. Hsu,et al. Bax in Murine Thymus Is a Soluble Monomeric Protein That Displays Differential Detergent-induced Conformations* , 1998, The Journal of Biological Chemistry.
[63] Nico Tjandra,et al. Structure of Bax Coregulation of Dimer Formation and Intracellular Localization , 2000, Cell.
[64] B. Antonsson,et al. 3,6-dibromocarbazole piperazine derivatives of 2-propanol as first inhibitors of cytochrome c release via Bax channel modulation. , 2003, Journal of medicinal chemistry.
[65] B. Corfe,et al. Cell Damage-induced Conformational Changes of the Pro-Apoptotic Protein Bak In Vivo Precede the Onset of Apoptosis , 1999, The Journal of cell biology.
[66] Jeffrey Robbins,et al. Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death , 2005, Nature.
[67] S. Orrenius,et al. Apoptosis: a basic biological phenomenon with wide‐ranging implications in human disease , 2005, Journal of internal medicine.
[68] M. Zoratti,et al. The giant channel of the inner mitochondrial membrane is inhibited by cyclosporin A. , 1991, The Journal of biological chemistry.
[69] R. Haworth,et al. The Ca2+-induced membrane transition in mitochondria. I. The protective mechanisms. , 1979, Archives of biochemistry and biophysics.
[70] S. Korsmeyer,et al. Effects of cytochrome c on the mitochondrial apoptosis-induced channel MAC. , 2004, American journal of physiology. Cell physiology.
[71] S. Korsmeyer,et al. A novel, high conductance channel of mitochondria linked to apoptosis in mammalian cells and Bax expression in yeast , 2001, The Journal of cell biology.
[72] Xiaodong Wang,et al. Induction of Apoptotic Program in Cell-Free Extracts: Requirement for dATP and Cytochrome c , 1996, Cell.
[73] P. Bernardi,et al. Properties of the Permeability Transition Pore in Mitochondria Devoid of Cyclophilin D* , 2005, Journal of Biological Chemistry.
[74] B. Antonsson,et al. Mitochondria and the Bcl-2 family proteins in apoptosis signaling pathways , 2004, Molecular and Cellular Biochemistry.
[75] R. Youle,et al. Control of mitochondrial permeability by Bcl-2 family members. , 2004, Biochimica et biophysica acta.
[76] Andy J. Minn,et al. Bcl-xL forms an ion channel in synthetic lipid membranes , 1997, Nature.
[77] 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.
[78] X. Roucou,et al. Bid induces cytochrome c-impermeable Bax channels in liposomes. , 2002, The Biochemical journal.
[79] W. Craigen,et al. Each mammalian mitochondrial outer membrane porin protein is dispensable: effects on cellular respiration. , 1999, Biochimica et biophysica acta.
[80] Junying Yuan,et al. Apoptosis in the nervous system , 2000, Nature.
[81] P. Nicotera,et al. Apoptosis and necrosis: different execution of the same death. , 1999, Biochemical Society symposium.
[82] R. Haworth,et al. The Ca2+-induced membrane transition in mitochondria. III. Transitional Ca2+ release. , 1979, Archives of biochemistry and biophysics.
[83] D. Allison,et al. Physiology: Does gut hormone PYY3–36 decrease food intake in rodents? , 2004, Nature.
[84] M. Zoratti,et al. The mitochondrial megachannel is the permeability transition pore , 1992, Journal of bioenergetics and biomembranes.
[85] D. J. Reed,et al. Cyclosporin A protects hepatocytes subjected to high Ca2+ and oxidative stress , 1992, FEBS letters.
[86] G. Bellot,et al. The Mitochondrial Apoptosis-induced Channel (MAC) Corresponds to a Late Apoptotic Event* , 2004, Journal of Biological Chemistry.
[87] M. King,et al. Two high conductance channels of the mitochondrial inner membrane are independent of the human mitochondrial genome , 1998, FEBS Letters.
[88] B. Stoica,et al. Ceramide induces neuronal apoptosis through mitogen-activated protein kinases and causes release of multiple mitochondrial proteins , 2005, Molecular and Cellular Neuroscience.
[89] P. Krammer,et al. CD95's deadly mission in the immune system , 2000, Nature.
[90] S. Martin,et al. The mitochondrial apoptosome: a killer unleashed by the cytochrome seas. , 2001, Trends in biochemical sciences.
[91] Xu Luo,et al. Endonuclease G is an apoptotic DNase when released from mitochondria , 2001, Nature.
[92] B. Zhivotovsky,et al. Role of apoptosis in pancreatic beta-cell death in diabetes. , 2001, Diabetes.
[93] D. Iacopetta,et al. A fourth ADP/ATP carrier isoform in man: identification, bacterial expression, functional characterization and tissue distribution , 2005, FEBS letters.
[94] P. Bernardi,et al. The permeability transition and BCL-2 family proteins in apoptosis: co-conspirators or independent agents? , 2006, Cell Death and Differentiation.
[95] Dean P. Jones,et al. The ADP/ATP translocator is not essential for the mitochondrial permeability transition pore , 2004, Nature.
[96] T. Gunter,et al. Mechanisms by which mitochondria transport calcium. , 1990, The American journal of physiology.
[97] Y. Antonenko,et al. Calcium modulation of mitochondrial inner membrane channel activity. , 1991, Biochemical and biophysical research communications.
[98] 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.
[99] R. Haworth,et al. The Ca2+-induced membrane transition in mitochondria. II. Nature of the Ca2+ trigger site. , 1979, Archives of biochemistry and biophysics.
[100] S. Korsmeyer,et al. Proapoptotic BAX and BAK: A Requisite Gateway to Mitochondrial Dysfunction and Death , 2001, Science.
[101] K. Kinnally,et al. Overexpression of Bcl‐2 suppresses the calcium activation of a mitochondrial megachannel , 2001, FEBS letters.