Cardioprotection and altered mitochondrial adenine nucleotide transport
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[1] W. Craigen,et al. Nek1 regulates cell death and mitochondrial membrane permeability through phosphorylation of VDAC1 , 2009, Cell cycle.
[2] E. Murphy,et al. Glycogen Synthase Kinase 3 Inhibition Slows Mitochondrial Adenine Nucleotide Transport and Regulates Voltage-Dependent Anion Channel Phosphorylation , 2008, Circulation research.
[3] J. Hoek,et al. Regulation of hexokinase binding to VDAC , 2008, Journal of bioenergetics and biomembranes.
[4] A. Shah,et al. Glycogen Synthase Kinase-3 Inactivation Is Not Required for Ischemic Preconditioning or Postconditioning in the Mouse , 2008, Circulation research.
[5] E. Murphy,et al. Does inhibition of glycogen synthase kinase protect in mice? , 2008, Circulation research.
[6] W. Craigen,et al. Genetic strategies for dissecting mammalian and Drosophila voltage-dependent anion channel functions , 2008, Journal of bioenergetics and biomembranes.
[7] G. Bhamra,et al. Metformin protects the ischemic heart by the Akt-mediated inhibition of mitochondrial permeability transition pore opening , 2008, Basic Research in Cardiology.
[8] S. Sollott,et al. Hexokinase II Detachment from Mitochondria Triggers Apoptosis through the Permeability Transition Pore Independent of Voltage-Dependent Anion Channels , 2008, PloS one.
[9] S. Miyamoto,et al. Akt mediates mitochondrial protection in cardiomyocytes through phosphorylation of mitochondrial hexokinase-II , 2008, Cell Death and Differentiation.
[10] K. Werdan,et al. Myocardial ischemia/reperfusion causes VDAC phosphorylation which is reduced by cardioprotection with a p38 MAP kinase inhibitor , 2007, Proteomics.
[11] A. Abellán,et al. Opening of mitochondrial permeability transition pore induces hypercontracture in Ca2+ overloaded cardiac myocytes , 2007, Basic Research in Cardiology.
[12] G. Derumeaux,et al. Inhibition of mitochondrial permeability transition improves functional recovery and reduces mortality following acute myocardial infarction in mice. , 2007, American journal of physiology. Heart and circulatory physiology.
[13] D. Yellon,et al. Reperfusion injury salvage kinase signalling: taking a RISK for cardioprotection , 2007, Heart Failure Reviews.
[14] Michael V. Cohen,et al. Signaling pathways in ischemic preconditioning , 2007, Heart Failure Reviews.
[15] C. Hoppel,et al. Post-translational modifications of rat liver mitochondrial outer membrane proteins identified by mass spectrometry. , 2007, Biochimica et biophysica acta.
[16] A. Hsu,et al. GSK3β inhibition and KATP channel opening mediate acute opioid-induced cardioprotection at reperfusion , 2007, Basic Research in Cardiology.
[17] W. Craigen,et al. Voltage-dependent anion channels are dispensable for mitochondrial-dependent cell death , 2007, Nature Cell Biology.
[18] B. Doble,et al. Glycogen synthase kinase-3--an overview of an over-achieving protein kinase. , 2006, Current drug targets.
[19] J. Soler‐Soler,et al. Mitochondrial Ca2+ uptake during simulated ischemia does not affect permeability transition pore opening upon simulated reperfusion. , 2006, Cardiovascular research.
[20] J. Lemasters,et al. Voltage-dependent anion channel (VDAC) as mitochondrial governator--thinking outside the box. , 2006, Biochimica et biophysica acta.
[21] J. Hoek,et al. Activation of glycogen synthase kinase 3beta disrupts the binding of hexokinase II to mitochondria by phosphorylating voltage-dependent anion channel and potentiates chemotherapy-induced cytotoxicity. , 2005, Cancer research.
[22] E. Murphy,et al. Inhibition of GSK-3β as a target for cardioprotection: the importance of timing, location, duration and degree of inhibition , 2005, Expert opinion on therapeutic targets.
[23] C. Thompson,et al. Hexokinase-mitochondria interaction mediated by Akt is required to inhibit apoptosis in the presence or absence of Bax and Bak. , 2004, Molecular cell.
[24] Michael D. Schneider,et al. Transgenic Expression of Bcl-2 Modulates Energy Metabolism, Prevents Cytosolic Acidification During Ischemia, and Reduces Ischemia/Reperfusion Injury , 2004, Circulation research.
[25] G. Grover,et al. Excessive ATP hydrolysis in ischemic myocardium by mitochondrial F1F0-ATPase: effect of selective pharmacological inhibition of mitochondrial ATPase hydrolase activity. , 2004, American journal of physiology. Heart and circulatory physiology.
[26] M. Duchen,et al. Preconditioning protects by inhibiting the mitochondrial permeability transition. , 2004, American journal of physiology. Heart and circulatory physiology.
[27] E. Olson,et al. Glycogen synthase kinase-3β mediates convergence of protection signaling to inhibit the mitochondrial permeability transition pore , 2004 .
[28] A. Hsu,et al. Opioid-Induced Cardioprotection Occurs via Glycogen Synthase Kinase β Inhibition During Reperfusion in Intact Rat Hearts , 2004, Circulation research.
[29] S. Javadov,et al. Mitochondrial permeability transition pore opening during myocardial reperfusion--a target for cardioprotection. , 2004, Cardiovascular research.
[30] S. Javadov,et al. Ischaemic Preconditioning Inhibits Opening of Mitochondrial Permeability Transition Pores in the Reperfused Rat Heart , 2003, The Journal of physiology.
[31] P. Ping,et al. Protein Kinase C&egr; Interacts With and Inhibits the Permeability Transition Pore in Cardiac Mitochondria , 2003, Circulation research.
[32] P. dos Santos,et al. Mechanisms by which opening the mitochondrial ATP- sensitive K(+) channel protects the ischemic heart. , 2002, American journal of physiology. Heart and circulatory physiology.
[33] E. Murphy,et al. Phosphorylation of Glycogen Synthase Kinase-3&bgr; During Preconditioning Through a Phosphatidylinositol-3-Kinase–Dependent Pathway Is Cardioprotective , 2002, Circulation research.
[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] E. Murphy,et al. Diazoxide-Induced Cardioprotection Requires Signaling Through a Redox-Sensitive Mechanism , 2001, Circulation research.
[36] 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.
[37] Masashi Narita,et al. Bcl-2 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDAC , 1999, Nature.
[38] M. Stern,et al. Mitochondrial membrane potential in single living adult rat cardiac myocytes exposed to anoxia or metabolic inhibition. , 1995, The Journal of physiology.
[39] A. Halestrap,et al. Mitochondrial non-specific pores remain closed during cardiac ischaemia, but open upon reperfusion. , 1995, The Biochemical journal.
[40] G. Asimakis,et al. Ischemic preconditioning attenuates acidosis and postischemic dysfunction in isolated rat heart. , 1992, The American journal of physiology.
[41] R. Jennings,et al. Effect of inhibition of the mitochondrial ATPase on net myocardial ATP in total ischemia. , 1991, Journal of molecular and cellular cardiology.
[42] R. Jennings,et al. Ischemic preconditioning slows energy metabolism and delays ultrastructural damage during a sustained ischemic episode. , 1990, Circulation research.
[43] R. Jennings,et al. Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. , 1986, Circulation.
[44] M. Colombini. VDAC: The channel at the interface between mitochondria and the cytosol , 2004, Molecular and Cellular Biochemistry.
[45] R. London,et al. Mechanism of preconditioning. Ionic alterations. , 1993, Circulation research.