Paul S Brookes

Summary

Affiliation: University of Rochester
Country: USA

Publications

  1. pmc A non-cardiomyocyte autonomous mechanism of cardioprotection involving the SLO1 BK channel
    Andrew P Wojtovich
    Department of Medicine, University of Rochester Medical Center, Rochester, NY, USA
    Peerj 1:e48. 2013
  2. ncbi request reprint Mitochondrial H(+) leak and ROS generation: an odd couple
    Paul S Brookes
    Department of Anesthesiology, University of Rochester, Medical Center Box 604, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Free Radic Biol Med 38:12-23. 2005
  3. ncbi request reprint Role of calcium and superoxide dismutase in sensitizing mitochondria to peroxynitrite-induced permeability transition
    Paul S Brookes
    Uiniversity of Alabama at Birmingham, Department of Pathology, 901 19th St South, Birmingham, AL 35294, USA
    Am J Physiol Heart Circ Physiol 286:H39-46. 2004
  4. ncbi request reprint A shortcut to mitochondrial signaling and pathology: a commentary on "Nonenzymatic formation of succinate in mitochondria under oxidative stress"
    Paul S Brookes
    Department of Anesthesiology, University of Rochester Medical Center, Box 604, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Free Radic Biol Med 41:41-5. 2006
  5. pmc Oxygen sensitivity of mitochondrial reactive oxygen species generation depends on metabolic conditions
    David L Hoffman
    Department of Biochemistry, University of Rochester Medical Center, Rochester, NY 14642, USA
    J Biol Chem 284:16236-45. 2009
  6. ncbi request reprint Reversible inhibition of cytochrome c oxidase by peroxynitrite proceeds through ascorbate-dependent generation of nitric oxide
    Maria Cecilia Barone
    Department of Pathology and Center for Free Radical Biology, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA
    J Biol Chem 278:27520-4. 2003
  7. pmc Cardioprotection and mitochondrial S-nitrosation: effects of S-nitroso-2-mercaptopropionyl glycine (SNO-MPG) in cardiac ischemia-reperfusion injury
    Sergiy M Nadtochiy
    Department of Anesthesiology, PO Box 604, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
    J Mol Cell Cardiol 42:812-25. 2007
  8. pmc SIRT1-mediated acute cardioprotection
    Sergiy M Nadtochiy
    Department of Anesthesiology, University of Rochester Medical Center, Rochester, New York 14642, USA
    Am J Physiol Heart Circ Physiol 301:H1506-12. 2011
  9. pmc In vivo cardioprotection by S-nitroso-2-mercaptopropionyl glycine
    Sergiy M Nadtochiy
    Department of Anesthesiology, University of Rochester Medical Center, Rochester, NY 14620, USA
    J Mol Cell Cardiol 46:960-8. 2009
  10. pmc Ischemic preconditioning: the role of mitochondria and aging
    Andrew P Wojtovich
    Department of Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA
    Exp Gerontol 47:1-7. 2012

Research Grants

Collaborators

Detail Information

Publications62

  1. pmc A non-cardiomyocyte autonomous mechanism of cardioprotection involving the SLO1 BK channel
    Andrew P Wojtovich
    Department of Medicine, University of Rochester Medical Center, Rochester, NY, USA
    Peerj 1:e48. 2013
    ..These results suggest that opening SLO1 protects the heart during IR injury, via a mechanism that involves intrinsic cardiac neurons. Cardiac neuronal ion channels may be useful therapeutic targets for eliciting cardioprotection...
  2. ncbi request reprint Mitochondrial H(+) leak and ROS generation: an odd couple
    Paul S Brookes
    Department of Anesthesiology, University of Rochester, Medical Center Box 604, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Free Radic Biol Med 38:12-23. 2005
    ..Herein the molecular basis of both ROS generation and H(+) leak will be reviewed and the consequences of their interaction for mitochondrial function discussed...
  3. ncbi request reprint Role of calcium and superoxide dismutase in sensitizing mitochondria to peroxynitrite-induced permeability transition
    Paul S Brookes
    Uiniversity of Alabama at Birmingham, Department of Pathology, 901 19th St South, Birmingham, AL 35294, USA
    Am J Physiol Heart Circ Physiol 286:H39-46. 2004
    ..These studies suggest protein targets revealed by Ca(2+) include dehydrogenases and CoA - containing enzymes. These data are discussed in the context of the role of mitochondria, Ca(2+), and ONOO(-) in apoptotic signaling...
  4. ncbi request reprint A shortcut to mitochondrial signaling and pathology: a commentary on "Nonenzymatic formation of succinate in mitochondria under oxidative stress"
    Paul S Brookes
    Department of Anesthesiology, University of Rochester Medical Center, Box 604, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Free Radic Biol Med 41:41-5. 2006
  5. pmc Oxygen sensitivity of mitochondrial reactive oxygen species generation depends on metabolic conditions
    David L Hoffman
    Department of Biochemistry, University of Rochester Medical Center, Rochester, NY 14642, USA
    J Biol Chem 284:16236-45. 2009
    ..Finally, the data set (see supplemental material) may be useful in the mathematical modeling of mitochondrial metabolism...
  6. ncbi request reprint Reversible inhibition of cytochrome c oxidase by peroxynitrite proceeds through ascorbate-dependent generation of nitric oxide
    Maria Cecilia Barone
    Department of Pathology and Center for Free Radical Biology, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA
    J Biol Chem 278:27520-4. 2003
    ..These observations are discussed in the context of ONOO-/ascorbate reactivity and the interaction of CcOX with reactive nitrogen species...
  7. pmc Cardioprotection and mitochondrial S-nitrosation: effects of S-nitroso-2-mercaptopropionyl glycine (SNO-MPG) in cardiac ischemia-reperfusion injury
    Sergiy M Nadtochiy
    Department of Anesthesiology, PO Box 604, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
    J Mol Cell Cardiol 42:812-25. 2007
    ..Overall these data suggest that mitochondrial S-nitrosation and complex I inhibition constitute a protective signaling pathway that is amenable to pharmacologic augmentation...
  8. pmc SIRT1-mediated acute cardioprotection
    Sergiy M Nadtochiy
    Department of Anesthesiology, University of Rochester Medical Center, Rochester, New York 14642, USA
    Am J Physiol Heart Circ Physiol 301:H1506-12. 2011
    ....
  9. pmc In vivo cardioprotection by S-nitroso-2-mercaptopropionyl glycine
    Sergiy M Nadtochiy
    Department of Anesthesiology, University of Rochester Medical Center, Rochester, NY 14620, USA
    J Mol Cell Cardiol 46:960-8. 2009
    ..Overall, these results are consistent with a role for mitochondrial S-nitrosation and complex I inhibition in the cardioprotective mechanism of IPC and SNO-MPG in vivo...
  10. pmc Ischemic preconditioning: the role of mitochondria and aging
    Andrew P Wojtovich
    Department of Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA
    Exp Gerontol 47:1-7. 2012
    ..This review will summarize the effects of aging on myocardial IR injury and discuss relevant and emerging strategies to protect against MI with an emphasis on mitochondrial function...
  11. pmc SLO-2 is cytoprotective and contributes to mitochondrial potassium transport
    Andrew P Wojtovich
    Department of Medicine, University of Rochester Medical Center, Rochester, New York, United States of America
    PLoS ONE 6:e28287. 2011
    ..These findings suggest that SLO2 contributes to protection from hypoxic injury by increasing the permeability of the mitochondrial inner membrane to K(+)...
  12. pmc The mitochondrial ATP-dependent Lon protease: a novel target in lymphoma death mediated by the synthetic triterpenoid CDDO and its derivatives
    Steven H Bernstein
    James P Wilmot Cancer Center, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Blood 119:3321-9. 2012
    ..Together, these findings suggest that Lon inhibition plays a contributory role in CDDO-induced lymphoma cell death, and support the concept that mitochondrial Lon is a novel anticancer drug target...
  13. ncbi request reprint Mitochondria, nitric oxide, and cardiovascular dysfunction
    Anup Ramachandran
    Department of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294, USA
    Free Radic Biol Med 33:1465-74. 2002
    ..The interaction of NO with the various mitochondrial respiratory complexes and the role NO plays in modulating mitochondrial-mediated apoptosis in these systems will be discussed...
  14. pmc Cardioprotection by metabolic shut-down and gradual wake-up
    Lindsay S Burwell
    Department of Biochemistry and Biophysics, University of Rochester Medical Center, Rochester, NY 14642, USA
    J Mol Cell Cardiol 46:804-10. 2009
    ..This paper will review the evidence in support of this hypothesis, with a focus on inhibition of each of the mitochondrial respiratory complexes...
  15. pmc Mechanisms of the interaction of nitroxyl with mitochondria
    Sruti Shiva
    Department of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294, USA
    Biochem J 379:359-66. 2004
    ....
  16. ncbi request reprint Control of mitochondrial respiration by NO*, effects of low oxygen and respiratory state
    Paul S Brookes
    Departments of Pathology, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA
    J Biol Chem 278:31603-9. 2003
    ..dependent spectral species in the respiratory chain in this state. These results are discussed in the context of regulation of respiration by NO. in vivo and its implications for the control of vessel-parenchymal O2 gradients...
  17. pmc The endogenous mitochondrial complex II inhibitor malonate regulates mitochondrial ATP-sensitive potassium channels: implications for ischemic preconditioning
    Andrew P Wojtovich
    Department of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, NY 14642, USA
    Biochim Biophys Acta 1777:882-9. 2008
    ..Together, these observations suggest that complex II inhibition by endogenously formed malonate may represent an important activation pathway for mK(ATP) channels during IPC...
  18. pmc Direct evidence for S-nitrosation of mitochondrial complex I
    Lindsay S Burwell
    Department of Anesthesiology, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14620, USA
    Biochem J 394:627-34. 2006
    ..The implications of these results for the physiological regulation of respiration, for reactive oxygen species generation and for a potential role of S-nitrosation in cardioprotection are discussed...
  19. pmc Physiological consequences of complex II inhibition for aging, disease, and the mKATP channel
    Andrew P Wojtovich
    Department of Medicine, University of Rochester Medical Center, Rochester, NY, USA
    Biochim Biophys Acta 1827:598-611. 2013
    ..This article is part of a Special Issue entitled: Respiratory complex II: Role in cellular physiology and disease...
  20. pmc Mitochondrial ATP-sensitive potassium channel activity and hypoxic preconditioning are independent of an inwardly rectifying potassium channel subunit in Caenorhabditis elegans
    Andrew P Wojtovich
    Department of Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA
    FEBS Lett 586:428-34. 2012
    ..These data suggest that the mK(ATP) in C. elegans does not arise from a Kir derived channel...
  21. pmc Different mechanisms of mitochondrial proton leak in ischaemia/reperfusion injury and preconditioning: implications for pathology and cardioprotection
    Sergiy M Nadtochiy
    Department of Anesthesiology, University of Rochester Medical Center, Rochester, NY 14642, USA
    Biochem J 395:611-8. 2006
    ..71). In conclusion, these data suggest that the modulation of H+ leak may have important implications for the outcome of IR injury...
  22. pmc A novel mitochondrial K(ATP) channel assay
    Andrew P Wojtovich
    Department of Pharmacology, University of Rochester Medical Center, 601 Elmwood Ave, Rochester, NY 14642, USA
    Circ Res 106:1190-6. 2010
    ..The validity of current methods to assay mK(ATP) activity is disputed...
  23. ncbi request reprint The mitochondrial complex II and ATP-sensitive potassium channel interaction: quantitation of the channel in heart mitochondria
    Andrew P Wojtovich
    Department of Anesthesiology, University of Rochester Medical Center, NY, USA
    Acta Biochim Pol 57:431-4. 2010
    ..4 % of total complex II molecules are necessary to activate the mK(ATP). These results estimate the mK(ATP) content at 15 channels per mitochondrion...
  24. ncbi request reprint Mitochondrial dysfunction in cardiac ischemia-reperfusion injury: ROS from complex I, without inhibition
    Andrew J Tompkins
    Departments of Anesthesiology, and Biochemistry and Molecular Biology, Box 604, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester NY 14642, USA
    Biochim Biophys Acta 1762:223-31. 2006
    ..These thiol modifications were accompanied by enhanced ROS generation from CxI, but not complex III. Implications for the pathology of cardiac I-R injury are discussed...
  25. pmc NDUFS4: creation of a mouse model mimicking a Complex I disorder
    Christopher A Ingraham
    Department of Biomedical Genetics, Univ of Rochester Medical Center, Rochester, NY, USA
    Mitochondrion 9:204-10. 2009
    ..Decreased Complex I activity with unaltered Complex II activity, along with an accumulation of lactate, were consistent with Complex I disorders in this mouse model...
  26. pmc Mitochondrial nitroalkene formation and mild uncoupling in ischaemic preconditioning: implications for cardioprotection
    Sergiy M Nadtochiy
    Department of Anesthesiology, Box 604, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Cardiovasc Res 82:333-40. 2009
    ....
  27. pmc p90 ribosomal S6 kinase regulates activity of the renin-angiotensin system: a pathogenic mechanism for ischemia-reperfusion injury
    Xi Shi
    Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14620, USA
    J Mol Cell Cardiol 51:272-5. 2011
    ..Thus, renin inhibition may provide an alternative therapeutic strategy under conditions of increased RAS...
  28. pmc Kir6.2 is not the mitochondrial KATP channel but is required for cardioprotection by ischemic preconditioning
    Andrew P Wojtovich
    Department of Medicine, University of Rochester Medical Center, Rochester, NY, USA
    Am J Physiol Heart Circ Physiol 304:H1439-45. 2013
    ..2(-/-) mice, suggesting no role for Kir6.2 in the mKATP. Collectively, these data indicate that Kir6.2 is required for the full response to IPC or diazoxide but is not involved in mKATP formation...
  29. pmc A cell-based phenotypic assay to identify cardioprotective agents
    Stephanie Guo
    School of Medicine, University of Rochester Medical Center, 601 Elmwood Ave, Rochester, NY 14642, USA
    Circ Res 110:948-57. 2012
    ..The lack of clinical therapies for IR injury may be partly due to the difficulty of adapting IR injury models to high-throughput screening (HTS)...
  30. pmc The complex II inhibitor atpenin A5 protects against cardiac ischemia-reperfusion injury via activation of mitochondrial KATP channels
    Andrew P Wojtovich
    Department of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, NY, USA
    Basic Res Cardiol 104:121-9. 2009
    ..In conclusion, the specific complex II inhibitor AA5 is the most potent mK(ATP) activator discovered to date, and provides a novel method of activating mK(ATP) channels and protecting the heart from IR injury...
  31. ncbi request reprint Purine release: a protective signaling mechanism of the mitochondrial permeability transition pore in ischemia
    Sergiy M Nadtochiy
    Department of Anesthesiology, University of Rochester Medical Center, Rochester, NY 14642, USA
    Fiziol Zh 54:5-14. 2008
    ..Both these events were inhibited by the PTP blockers cyclosporin A and sanglifehrin A. Implications for cardioprotective signaling by purines and the PTP are discussed...
  32. pmc Modulation of cell surface protein free thiols: a potential novel mechanism of action of the sesquiterpene lactone parthenolide
    Jolanta Skalska
    James P Wilmot Cancer Center, University of Rochester Medical Center, Rochester, New York, United States of America
    PLoS ONE 4:e8115. 2009
    ..Given recent data to suggest that the redox status of extracellular protein thiol groups (i.e. exofacial thiols) effects cell behavior, we hypothesized that redox active anti-cancer agents would modulate exofacial protein thiols...
  33. ncbi request reprint Calcium, ATP, and ROS: a mitochondrial love-hate triangle
    Paul S Brookes
    University of Rochester Medical Center, 601 Elmwood Ave, Box 711, Rochester, NY 14642, USA
    Am J Physiol Cell Physiol 287:C817-33. 2004
    ..Overall, a "two-hit" hypothesis is developed, in which Ca(2+) plus another pathological stimulus can bring about mitochondrial dysfunction...
  34. pmc The C. elegans mitochondrial K+(ATP) channel: a potential target for preconditioning
    Andrew P Wojtovich
    Department of Pharmacology and Physiology, Box 604, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Biochem Biophys Res Commun 376:625-8. 2008
    ..Since C. elegans also exhibit IPC, our observations provide a framework to study the role of mK(ATP) in IR injury in a genetic model organism...
  35. ncbi request reprint High throughput two-dimensional blue-native electrophoresis: a tool for functional proteomics of mitochondria and signaling complexes
    Paul S Brookes
    Department of Pathology, University of Alabama at Birmingham, Biomedical Research Building 2, 901 19th Street South, Birmingham, AL 35294, USA
    Proteomics 2:969-77. 2002
    ..Applications of this functional mitochondrial proteomics method are discussed...
  36. ncbi request reprint Response of mitochondrial reactive oxygen species generation to steady-state oxygen tension: implications for hypoxic cell signaling
    David L Hoffman
    Box 604 Anesthesiology, Univ of Rochester Medical Center, 601 Elmwood Ave, Rochester, NY 14642, USA
    Am J Physiol Heart Circ Physiol 292:H101-8. 2007
    ..The implications for hypoxic cell signaling are discussed...
  37. ncbi request reprint Chronic alcohol consumption increases the sensitivity of rat liver mitochondrial respiration to inhibition by nitric oxide
    Aparna Venkatraman
    Department of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294, USA
    Hepatology 38:141-7. 2003
    ..We propose that this results in a greater vulnerability to hypoxia and the development of alcohol-induced hepatotoxicity...
  38. ncbi request reprint Mitochondrial Dok-4 recruits Src kinase and regulates NF-kappaB activation in endothelial cells
    Seigo Itoh
    Center for Cardiovascular Research, University of Rochester, Rochester, New York 14642, USA
    J Biol Chem 280:26383-96. 2005
    ..These data suggest a role for mitochondrial Dok-4 as an anchoring molecule for the tyrosine kinase c-Src, and in turn as a regulator of TNF-alpha-mediated ROS production and NF-kappaB activation...
  39. pmc An analysis of the effects of Mn2+ on oxidative phosphorylation in liver, brain, and heart mitochondria using state 3 oxidation rate assays
    Thomas E Gunter
    Department of Biochemistry and Biophysics, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA
    Toxicol Appl Pharmacol 249:65-75. 2010
    ....
  40. pmc Nitroalkenes confer acute cardioprotection via adenine nucleotide translocase 1
    Sergiy M Nadtochiy
    Department of Anesthesiology, University of Rochester Medical Center, Rochester, New York 14642, USA
    J Biol Chem 287:3573-80. 2012
    ..Although the molecular mechanism linking ANT1-Cys(57) nitroalkylation and uncoupling is not yet known, these data suggest that ANT1-mediated uncoupling may be a mechanism for nitroalkene-induced cardioprotection...
  41. ncbi request reprint Measurement of mitochondrial respiratory thresholds and the control of respiration by nitric oxide
    Paul S Brookes
    Department of Pathology, University of Alabama, Birmingham, Alabama 35294, USA
    Methods Enzymol 359:305-19. 2002
    ..Such experiments can provide insight into the intricate nature of the interaction between NO. and mitochondria and the variations in this system that can occur under both physiological and pathological conditions...
  42. pmc SIRT1 is a redox-sensitive deacetylase that is post-translationally modified by oxidants and carbonyl stress
    Samuel Caito
    Department of Environmental Medicine, University of Rochester Medical Center, 601 Elmwood Ave, Box 850, Rochester, NY 14642, USA
    FASEB J 24:3145-59. 2010
    ..Our data suggest that oxidants/aldehydes covalently modify SIRT1, decreasing enzymatic activity and marking the protein for proteasomal degradation, which has implications in inflammatory conditions...
  43. pmc Mitochondrial biotransformation of omega-(phenoxy)alkanoic acids, 3-(phenoxy)acrylic acids, and omega-(1-methyl-1H-imidazol-2-ylthio)alkanoic acids: a prodrug strategy for targeting cytoprotective antioxidants to mitochondria
    Kurt S Roser
    Mitochondrial Research and Innovation Group, Department of Anesthesiology, Rochester, NY 14642, USA
    Bioorg Med Chem 18:1441-8. 2010
    ..These results demonstrate that mitochondrial beta-oxidation is a potentially useful delivery system for targeting antioxidants to mitochondria...
  44. ncbi request reprint The triterpenoid 2-cyano-3,12-dioxooleana-1,9-dien-28-oic acid and its derivatives elicit human lymphoid cell apoptosis through a novel pathway involving the unregulated mitochondrial permeability transition pore
    Paul S Brookes
    Department of Anesthesiology, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Cancer Res 67:1793-802. 2007
    ....
  45. ncbi request reprint Mitochondria as a target for the cardioprotective effects of nitric oxide in ischemia-reperfusion injury
    Lindsay S Burwell
    Department of Biochemistry and Biophysics, University of Rochester Medical Center, Rochester, New York 14642, USA
    Antioxid Redox Signal 10:579-99. 2008
    ..These direct effects of NO* on mitochondria are the focus of this review...
  46. ncbi request reprint Mitochondria: regulators of signal transduction by reactive oxygen and nitrogen species
    Paul S Brookes
    Department of Pathology and Center for Free Radical Biology, University of Alabama at Birmingham, Birmingham, AL 35294, USA
    Free Radic Biol Med 33:755-64. 2002
    ....
  47. ncbi request reprint Intra-myocyte ion homeostasis during ischemia-reperfusion injury: effects of pharmacologic preconditioning and controlled reperfusion
    James E Davies
    Department of Surgery, Birmingham, University of Alabama at Birmingham, 35294, USA
    Ann Thorac Surg 76:1252-8; discussion 1258. 2003
    ..This study determines whether controlled reperfusion or diazoxide improves intramyocyte Na(+) homeostasis using a porcine model of severe ischemia-reperfusion injury...
  48. pmc The coordinated increased expression of biliverdin reductase and heme oxygenase-2 promotes cardiomyocyte survival: a reductase-based peptide counters β-adrenergic receptor ligand-mediated cardiac dysfunction
    Bo Ding
    University of Rochester School of Medicine and Dentistry, Department of Biochemistry and Biophysics, Rochester, NY 14642, USA
    FASEB J 25:301-13. 2011
    ..Finding that BVR and HO-2 levels, myocyte apoptosis, and contractile function of the heart can be modulated by small human BVR-based peptides offers a promising therapeutic approach for treatment of cardiac dysfunctions...
  49. pmc Lysine deacetylation in ischaemic preconditioning: the role of SIRT1
    Sergiy M Nadtochiy
    Department of Anesthesiology, University of Rochester Medical Center, 601 Elmwood Avenue, Box 604, Rochester, NY 14642, USA
    Cardiovasc Res 89:643-9. 2011
    ..Lysine (Lys) acetylation is an important regulator of protein function, but this type of modification has not been studied in the context of IPC. We investigated Lys acetylation in IPC and its upstream regulation by SIRT1...
  50. ncbi request reprint Modulation of mitochondrial adenosine triphosphate-sensitive potassium channels and sodium-hydrogen exchange provide additive protection from severe ischemia-reperfusion injury
    Stanley B Digerness
    Department of Surgery, University of Alabama at Birmingham, Birmingham, Ala 35294 0007, USA
    J Thorac Cardiovasc Surg 125:863-71. 2003
    ....
  51. doi request reprint Role of p90(RSK) in regulating the Crabtree effect: implications for cancer
    Emily K Redman
    School of Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Biochem Soc Trans 41:124-6. 2013
    ..Furthermore, preliminary data are presented suggesting a role for p90(RSK) and its upstream components, the ERK (extracellular-signal-regulated kinase) family of MAPKs (mitogen-activated protein kinases), in the Crabtree effect...
  52. pmc BCL-2 inhibition targets oxidative phosphorylation and selectively eradicates quiescent human leukemia stem cells
    Eleni D Lagadinou
    James P Wilmot Cancer Center, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Cell Stem Cell 12:329-41. 2013
    ..Based on these findings, we propose a model wherein the unique physiology of ROS-low LSCs provides an opportunity for selective targeting via disruption of BCL-2-dependent oxidative phosphorylation...
  53. pmc Mitochondria as a drug target in ischemic heart disease and cardiomyopathy
    Andrew M Walters
    School of Medicine and Dentistry, University of Rochester Medical Center, Rochester, NY 14642, USA
    Circ Res 111:1222-36. 2012
    ..This review summarizes efforts to date in targeting mitochondria for ischemic heart disease and cardiomyopathy therapy and outlines emerging drug targets in this field...
  54. ncbi request reprint Mitochondrial function in response to cardiac ischemia-reperfusion after oral treatment with quercetin
    Paul S Brookes
    Department of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294 2180, USA
    Free Radic Biol Med 32:1220-8. 2002
    ..These results indicate that oral low dose quercetin is cardioprotective, possibly via a mechanism involving protection of mitochondrial function during I-R...
  55. ncbi request reprint Specific modification of mitochondrial protein thiols in response to oxidative stress: a proteomics approach
    Tsu Kung Lin
    Department of Biochemistry, University of Otago, Box 56, Dunedin, New Zealand
    J Biol Chem 277:17048-56. 2002
    ..In addition the methodology has the potential to identify novel redox-dependent modulation of mitochondrial proteins...
  56. pmc Nitrite augments tolerance to ischemia/reperfusion injury via the modulation of mitochondrial electron transfer
    Sruti Shiva
    Vascular Medicine Branch, National Heart Lung Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
    J Exp Med 204:2089-102. 2007
    ..These data suggest that nitrite dynamically modulates mitochondrial resilience to reperfusion injury and may represent an effector of the cell-survival program of ischemic preconditioning and the Mediterranean diet...
  57. ncbi request reprint Oxidation of 10-formyltetrahydrofolate to 10-formyldihydrofolate by complex IV of rat mitochondria
    Paul S Brookes
    Department of Pathology and Department of Nutrition Sciences, University of Alabama at Birmingham, 35294, USA
    Biochemistry 41:5633-6. 2002
    ....
  58. ncbi request reprint Nanotransducers in cellular redox signaling: modification of thiols by reactive oxygen and nitrogen species
    Chris E Cooper
    Dept of Biological Sciences, University of Essex, Wivenhoe Park, CO4 3SQ, Colchester, UK
    Trends Biochem Sci 27:489-92. 2002
    ..The findings offer the enticing possibility that the cell can distinguish between different degrees of oxidant and nitrosative exposure by modification at a single site on a signaling molecule...
  59. pmc The basal proton conductance of mitochondria depends on adenine nucleotide translocase content
    Martin D Brand
    Medical Research Council Dunn Human Nutrition Unit, Hills Road, Cambridge CB2 2XY, UK
    Biochem J 392:353-62. 2005
    ..We conclude that half to two-thirds of the basal proton conductance of mitochondria is catalysed by the adenine nucleotide carrier, independently of its ATP/ADP exchange or fatty-acid-dependent proton-leak functions...
  60. ncbi request reprint Methods for measuring the regulation of respiration by nitric oxide
    Sruti Shiva
    Vascular Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Methods Cell Biol 80:395-416. 2007
  61. ncbi request reprint Characterization of weight loss and weight regain mechanisms after Roux-en-Y gastric bypass in rats
    Ana Guijarro
    Dept of Surgery, University Hospital, 750 East Adams St, Syracuse, NY 13210, USA
    Am J Physiol Regul Integr Comp Physiol 293:R1474-89. 2007
    ..These events override the compensatory response to the drop in leptin levels aimed at conserving energy...
  62. pmc Sustained weight loss after Roux-en-Y gastric bypass is characterized by down regulation of endocannabinoids and mitochondrial function
    Ana Guijarro
    Surgical Metabolism and Nutrition Laboratory, Neuroscience Program, Department of Surgery, University Hospital, SUNY Upstate Medical University, Syracuse, New York 13210, USA
    Ann Surg 247:779-90. 2008
    ..To determine the physiologic importance of endocannabinoids and mitochondrial function in the long-term outcome using a rat model of Roux-en-Y gastric bypass (RYGB) surgery...

Research Grants8

  1. Mitochondria & NO in Cardiac Ischemia-Reperfusion
    Paul Brookes; Fiscal Year: 2006
    ..Realization of these aims will greatly enhance understanding of the basic mechanisms underlying mitochondrial perturbations in I-R leading to novel therapies. ..
  2. Mitochondria and NO? in Cardiac Ischemic Preconditioning
    Paul Brookes; Fiscal Year: 2009
    ..It is anticipated that addressing Aims 1 & 2 will define new mechanisms by which NO mediates cardioprotection, and that Aim 3 will lead to novel therapies for the treatment of cardiac IR injury. ..
  3. Mitochondria and NO? in Cardiac Ischemic Preconditioning
    Paul S Brookes; Fiscal Year: 2010
    ..It is anticipated that addressing Aims 1 &2 will define new mechanisms by which NO mediates cardioprotection, and that Aim 3 will lead to novel therapies for the treatment of cardiac IR injury. ..
  4. C. Elegans and Mitochondrial K+ Channels
    KEITH W NEHRKE; Fiscal Year: 2010
    ..elegans. The identification of these molecules will help in the development of new therapies for heart attack and stroke. ..