In aging, the vulnerability of rat brain mitochondria is enhanced due to reduced level of 2′,3′-cyclic nucleotide-3′-phosphodiesterase (CNP) and subsequently increased permeability transition in brain mitochondria in old animals

[1]  G. Reiser,et al.  Functions of the neuron-specific protein ADAP1 (centaurin-α1) in neuronal differentiation and neurodegenerative diseases, with an overview of structural and biochemical properties of ADAP1 , 2014, Biological chemistry.

[2]  P. Kochanek,et al.  Role of CNPase in the oligodendrocytic extracellular 2′,3′‐cAMP‐adenosine pathway , 2013, Glia.

[3]  W. Kühlbrandt,et al.  Age-dependent dissociation of ATP synthase dimers and loss of inner-membrane cristae in mitochondria , 2013, Proceedings of the National Academy of Sciences.

[4]  P. Bernardi.  The mitochondrial permeability transition pore: a mystery solved? , 2013, Front. Physiol..

[5]  V. Giorgio,et al.  Dimers of mitochondrial ATP synthase form the permeability transition pore , 2013, Proceedings of the National Academy of Sciences.

[6]  M. Colombini.  VDAC structure, selectivity, and dynamics. , 2012, Biochimica et biophysica acta.

[7]  S. Heckers,et al.  A myelin gene causative of a catatonia-depression syndrome upon aging , 2012, EMBO molecular medicine.

[8]  P. Kochanek,et al.  The brain in vivo expresses the 2′,3′‐cAMP‐adenosine pathway , 2012, Journal of neurochemistry.

[9]  S. Bezrukov,et al.  VDAC inhibition by tubulin and its physiological implications. , 2012, Biochimica et biophysica acta.

[10]  E. Jackson.  The 2',3'-cAMP-adenosine pathway. , 2011, American journal of physiology. Renal physiology.

[11]  G. Reiser,et al.  The mitochondria permeability transition pore complex in the brain with interacting proteins – promising targets for protection in neurodegenerative diseases , 2010, Biological chemistry.

[12]  L. Martin.  Mitochondrial and Cell Death Mechanisms in Neurodegenerative Diseases , 2010, Pharmaceuticals.

[13]  E. Jackson,et al.  Extracellular 2′,3′-cAMP Is a Source of Adenosine* , 2009, The Journal of Biological Chemistry.

[14]  G. Reiser,et al.  The brain‐specific protein, p42IP4 (ADAP 1) is localized in mitochondria and involved in regulation of mitochondrial Ca2+ , 2009, Journal of neurochemistry.

[15]  G. Reiser,et al.  Ca2+-dependent permeability transition regulation in rat brain mitochondria by 2',3'-cyclic nucleotides and 2',3'-cyclic nucleotide 3'-phosphodiesterase. , 2009, American journal of physiology. Cell physiology.

[16]  D. Sackett,et al.  Tubulin binding blocks mitochondrial voltage-dependent anion channel and regulates respiration , 2008, Proceedings of the National Academy of Sciences.

[17]  A. Halestrap,et al.  The Mitochondrial Phosphate Carrier Interacts with Cyclophilin D and May Play a Key Role in the Permeability Transition* , 2008, Journal of Biological Chemistry.

[18]  G. Reiser,et al.  RanBPM, a novel interaction partner of the brain‐specific protein p42IP4/centaurin α‐1 , 2008, Journal of neurochemistry.

[19]  M. Mattson,et al.  The Identity and Regulation of the Mitochondrial Permeability Transition Pore , 2008, Annals of the New York Academy of Sciences.

[20]  R. Vakkalanka,et al.  Expression of oligodendrocyte-associated genes in dorsolateral prefrontal cortex of patients with schizophrenia , 2008, Schizophrenia Research.

[21]  V. Papadopoulos,et al.  The peripheral-type benzodiazepine receptor is involved in control of Ca2+-induced permeability transition pore opening in rat brain mitochondria. , 2007, Cell calcium.

[22]  W. Craigen,et al.  Voltage-dependent anion channels are dispensable for mitochondrial-dependent cell death , 2007, Nature Cell Biology.

[23]  M. Beal,et al.  Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases , 2006, Nature.

[24]  V. Shoshan-Barmatz,et al.  The voltage-dependent anion channel (VDAC): function in intracellular signalling, cell life and cell death. , 2006, Current pharmaceutical design.

[25]  A. Vinogradov,et al.  Generation of superoxide by the mitochondrial Complex I. , 2006, Biochimica et biophysica acta.

[26]  P. Braun,et al.  Mitochondrial localization of CNP2 is regulated by phosphorylation of the N-terminal targeting signal by PKC: Implications of a mitochondrial function for CNP2 in glial and non-glial cells , 2006, Molecular and Cellular Neuroscience.

[27]  P. Bernardi,et al.  Mitochondrial function and myocardial aging. A critical analysis of the role of permeability transition. , 2005, Cardiovascular research.

[28]  Jeffrey Robbins,et al.  Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death , 2005, Nature.

[29]  M. MacDonald,et al.  Striatal cells from mutant huntingtin knock-in mice are selectively vulnerable to mitochondrial complex II inhibitor-induced cell death through a non-apoptotic pathway. , 2004, Human molecular genetics.

[30]  Dean P. Jones,et al.  The ADP/ATP translocator is not essential for the mitochondrial permeability transition pore , 2004, Nature.

[31]  G. Reiser,et al.  Physiological Ca2+ level and Ca2+-induced Permeability Transition Pore control protein phosphorylation in rat brain mitochondria. , 2003, Cell calcium.

[32]  J. Wolff,et al.  2′,3′-Cyclic nucleotide 3′-phosphodiesterase: A membrane-bound, microtubule-associated protein and membrane anchor for tubulin , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[33]  S. Su,et al.  Loss of Preconditioning by Attenuated Activation of Myocardial ATP-Sensitive Potassium Channels in Elderly Patients Undergoing Coronary Angioplasty , 2002, Circulation.

[34]  M. Mather,et al.  Aging Enhances the Activation of the Permeability Transition Pore in Mitochondria , 2001, TheScientificWorldJournal.

[35]  S. Pepe.  Mitochondrial Function In Ischaemia And Reperfusion Of The Ageing Heart , 2000, Clinical and experimental pharmacology & physiology.

[36]  R. S. Sohal,et al.  Mitochondrial adenine nucleotide translocase is modified oxidatively during aging. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[37]  U. Walter,et al.  cDNA cloning of porcine p42IP4, a membrane‐associated and cytosolic 42 kDa inositol(1,3,4,5)tetrakisphosphate receptor from pig brain with similarly high affinity for phosphatidylinositol (3,4,5)P3 , 1997, FEBS letters.

[38]  B. Van Houten,et al.  Mitochondrial DNA damage is more extensive and persists longer than nuclear DNA damage in human cells following oxidative stress. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[39]  M. Beal,et al.  Aging, energy, and oxidative stress in neurodegenerative diseases , 1995, Annals of neurology.

[40]  M. Zoratti,et al.  The mitochondrial permeability transition. , 1995, Biochimica et biophysica acta.

[41]  D. Wallace,et al.  Mitochondrial DNA mutations in human degenerative diseases and aging. , 1995, Biochimica et biophysica acta.

[42]  G. Reiser,et al.  Generation of a monoclonal antibody against the myelin protein CNP (2′,3′-cyclic nucleotide 3′-phosphodiesterase) suitable for biochemical and for immunohistochemical investigations of CNP , 1994, Neurochemical Research.

[43]  R. Raines,et al.  Energetics of catalysis by ribonucleases: fate of the 2',3'-cyclic phosphodiester intermediate. , 1994, Biochemistry.

[44]  N. Sims.  Rapid Isolation of Metabolically Active Mitochondria from Rat Brain and Subregions Using Percoll Density Gradient Centrifugation , 1990, Journal of neurochemistry.

[45]  N. Hilschmann,et al.  [Identification of human porins. I. Purification of a porin from human B-lymphocytes (Porin 31HL) and the topochemical proof of its expression on the plasmalemma of the progenitor cell]. , 1989, Biological chemistry Hoppe-Seyler.

[46]  J. Bradbury,et al.  Photoaffinity labelling of central-nervous-system myelin. Evidence for an endogenous type I cyclic AMP-dependent kinase phosphorylating the larger subunit of 2',3'-cyclic nucleotide 3'-phosphodiesterase. , 1984, The Biochemical journal.

[47]  B Chance,et al.  Hydroperoxide metabolism in mammalian organs. , 1979, Physiological reviews.

[48]  C. Chinopoulos,et al.  Modulation of the mitochondrial permeability transition by cyclophilin D: moving closer to F(0)-F(1) ATP synthase? , 2012, Mitochondrion.

[49]  Keilin Memorial Lecture.  A pore way to die: the role of mitochondria in reperfusion injury and cardioprotection , 2010 .

[50]  J. Hinman,et al.  Age‐dependent accumulation of ubiquitinated 2′,3′‐cyclic nucleotide 3′‐phosphodiesterase in myelin lipid rafts , 2008, Glia.

[51]  Lorenzo Galluzzi,et al.  Mitochondrial membrane permeabilization in cell death. , 2007, Physiological reviews.

[52]  S. Papa,et al.  Reactive oxygen species, mitochondria, apoptosis and aging , 2004, Molecular and Cellular Biochemistry.