Shane R Thomas

Summary

Affiliation: University of New South Wales
Country: Australia

Publications

  1. ncbi Redox control of endothelial function and dysfunction: molecular mechanisms and therapeutic opportunities
    Shane R Thomas
    Centre for Vascular Research, School of Medical Sciences, University of New South Wales, Sydney, NSW 2052, Australia
    Antioxid Redox Signal 10:1713-65. 2008
  2. ncbi Post-translational regulation of human indoleamine 2,3-dioxygenase activity by nitric oxide
    Shane R Thomas
    Centre for Vascular Research, Faculty of Medicine, University of New South Wales, Sydney 2052, Australia
    J Biol Chem 282:23778-87. 2007
  3. ncbi Hydrogen peroxide restrains endothelium-derived nitric oxide bioactivity -- role for iron-dependent oxidative stress
    Shane R Thomas
    Evans Memorial Department of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    Free Radic Biol Med 41:681-8. 2006
  4. ncbi Activation of endothelial nitric-oxide synthase by the p38 MAPK in response to black tea polyphenols
    Elad Anter
    Evans Memorial Department of Medicine, The Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachussetts 02118, USA
    J Biol Chem 279:46637-43. 2004
  5. ncbi Hypochlorous acid impairs endothelium-derived nitric oxide bioactivity through a superoxide-dependent mechanism
    Roland Stocker
    Evans Memorial Department of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Mass 02118, USA
    Arterioscler Thromb Vasc Biol 24:2028-33. 2004
  6. ncbi Human indoleamine 2,3-dioxygenase is a catalyst of physiological heme peroxidase reactions: implications for the inhibition of dioxygenase activity by hydrogen peroxide
    Mohammed Freewan
    Centre for Vascular Research and School of Medical Sciences, University of New South Wales, Sydney, New South Wales 2052, Australia
    J Biol Chem 288:1548-67. 2013
  7. ncbi Cytochrome b5, not superoxide anion radical, is a major reductant of indoleamine 2,3-dioxygenase in human cells
    Ghassan J Maghzal
    Centre for Vascular Research and Molecular Immunopathology Unit, Bosch Institute and Discipline of Pathology, School of Medical Sciences, University of Sydney, Sydney, New South Wales 2006, Australia
    J Biol Chem 283:12014-25. 2008
  8. ncbi Oxidative stress and endothelial nitric oxide bioactivity
    Shane R Thomas
    Whitaker Cardiovascular Institute, Boston University School of Medicine, 715 Albany Street, Room W507, Boston, MA 02118, U.S.A
    Antioxid Redox Signal 5:181-94. 2003
  9. ncbi Flavivirus infection induces indoleamine 2,3-dioxygenase in human monocyte-derived macrophages via tumor necrosis factor and NF-κB
    Amanda W S Yeung
    Centre for Vascular Research and School of Medical Sciences, The University of New South Wales, Sydney, Australia
    J Leukoc Biol 91:657-66. 2012
  10. ncbi L-Homocysteine and L-homocystine stereospecifically induce endothelial nitric oxide synthase-dependent lipid peroxidation in endothelial cells
    Stanley J Heydrick
    Evans Department of Medicine and Whitaker Cardiovascular Institute, Boston University, School of Medicine, Boston, MA 02118, USA
    Free Radic Biol Med 36:632-40. 2004

Collaborators

Detail Information

Publications23

  1. ncbi Redox control of endothelial function and dysfunction: molecular mechanisms and therapeutic opportunities
    Shane R Thomas
    Centre for Vascular Research, School of Medical Sciences, University of New South Wales, Sydney, NSW 2052, Australia
    Antioxid Redox Signal 10:1713-65. 2008
    ....
  2. ncbi Post-translational regulation of human indoleamine 2,3-dioxygenase activity by nitric oxide
    Shane R Thomas
    Centre for Vascular Research, Faculty of Medicine, University of New South Wales, Sydney 2052, Australia
    J Biol Chem 282:23778-87. 2007
    ..Reversible inhibition by NO may represent an important mechanism in controlling the immune regulatory actions of IDO...
  3. ncbi Hydrogen peroxide restrains endothelium-derived nitric oxide bioactivity -- role for iron-dependent oxidative stress
    Shane R Thomas
    Evans Memorial Department of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    Free Radic Biol Med 41:681-8. 2006
    ..The study highlights another way in which oxidative stress may impair NO bioactivity during vascular disease...
  4. ncbi Activation of endothelial nitric-oxide synthase by the p38 MAPK in response to black tea polyphenols
    Elad Anter
    Evans Memorial Department of Medicine, The Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachussetts 02118, USA
    J Biol Chem 279:46637-43. 2004
    ..Taken together, these data identify the p38 MAPK as an upstream component of Akt-mediated eNOS activation...
  5. ncbi Hypochlorous acid impairs endothelium-derived nitric oxide bioactivity through a superoxide-dependent mechanism
    Roland Stocker
    Evans Memorial Department of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Mass 02118, USA
    Arterioscler Thromb Vasc Biol 24:2028-33. 2004
    ..These data provide another mechanism whereby myeloperoxidase-derived oxidants can contribute to the impairment of NO bioactivity that is characteristic of atherosclerosis...
  6. ncbi Human indoleamine 2,3-dioxygenase is a catalyst of physiological heme peroxidase reactions: implications for the inhibition of dioxygenase activity by hydrogen peroxide
    Mohammed Freewan
    Centre for Vascular Research and School of Medical Sciences, University of New South Wales, Sydney, New South Wales 2052, Australia
    J Biol Chem 288:1548-67. 2013
    ..Peroxidase-mediated dioxygenase inactivation, NO consumption, or protein nitration may modulate the biological actions of IDO expressed in inflammatory tissues where the levels of H(2)O(2) and NO are elevated and l-Trp is low...
  7. ncbi Cytochrome b5, not superoxide anion radical, is a major reductant of indoleamine 2,3-dioxygenase in human cells
    Ghassan J Maghzal
    Centre for Vascular Research and Molecular Immunopathology Unit, Bosch Institute and Discipline of Pathology, School of Medical Sciences, University of Sydney, Sydney, New South Wales 2006, Australia
    J Biol Chem 283:12014-25. 2008
    ..Together, our data show that cytochrome b(5) rather than O(2)(*-) plays a major role in the activation of IDO in human cells...
  8. ncbi Oxidative stress and endothelial nitric oxide bioactivity
    Shane R Thomas
    Whitaker Cardiovascular Institute, Boston University School of Medicine, 715 Albany Street, Room W507, Boston, MA 02118, U.S.A
    Antioxid Redox Signal 5:181-94. 2003
    ..This review outlines how different forms of oxidative stress can impact on NO bioactivity and discusses strategies to prevent oxidative stress-induced endothelial dysfunction...
  9. ncbi Flavivirus infection induces indoleamine 2,3-dioxygenase in human monocyte-derived macrophages via tumor necrosis factor and NF-κB
    Amanda W S Yeung
    Centre for Vascular Research and School of Medical Sciences, The University of New South Wales, Sydney, Australia
    J Leukoc Biol 91:657-66. 2012
    ..Together, these data support that although IDO is not required by MDM for the clearance of established viral infection, the spread of flavivirus infection is limited by IDO expressed in uninfected, neighboring cells...
  10. ncbi L-Homocysteine and L-homocystine stereospecifically induce endothelial nitric oxide synthase-dependent lipid peroxidation in endothelial cells
    Stanley J Heydrick
    Evans Department of Medicine and Whitaker Cardiovascular Institute, Boston University, School of Medicine, Boston, MA 02118, USA
    Free Radic Biol Med 36:632-40. 2004
    ..Thus, homocyst(e)ine actively promotes oxidative stress in endothelial cells via an eNOS-dependent mechanism...
  11. ncbi Mitochondrial function is required for hydrogen peroxide-induced growth factor receptor transactivation and downstream signaling
    Kai Chen
    Evans Memorial Department of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, 715 Albany Street, MA 02118, USA
    J Biol Chem 279:35079-86. 2004
    ..These data establish a novel role for the mitochondrion as a proximal target specific to H(2)O(2)-induced signaling and growth factor transactivation...
  12. ncbi Hydrogen peroxide activates endothelial nitric-oxide synthase through coordinated phosphorylation and dephosphorylation via a phosphoinositide 3-kinase-dependent signaling pathway
    Shane R Thomas
    Evans Memorial Department of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts 02118. USA
    J Biol Chem 277:6017-24. 2002
    ..This response may represent an attempt by endothelial cells to maintain NO bioactivity under conditions of enhanced oxidative stress...
  13. ncbi Processes involved in the site-specific effect of probucol on atherosclerosis in apolipoprotein E gene knockout mice
    Katherine Choy
    Centre for Vascular Research, University of New South Wales, Sydney, Australia
    Arterioscler Thromb Vasc Biol 25:1684-90. 2005
    ..To elucidate processes by which the antioxidant probucol increases lesion size at the aortic sinus and decreases atherosclerosis at more distal sites in apolipoprotein E-deficient (apoE(-/-)) mice...
  14. ncbi Kynurenine is an endothelium-derived relaxing factor produced during inflammation
    Yutang Wang
    Centre for Vascular Research, School of Medical Sciences Pathology and Bosch Institute, Faculty of Medicine, University of Sydney, Sydney, Australia
    Nat Med 16:279-85. 2010
    ..Kynurenine administration decreased blood pressure in a dose-dependent manner in spontaneously hypertensive rats. Our results identify tryptophan metabolism by Ido as a new pathway contributing to the regulation of vascular tone...
  15. ncbi Sustained expression of heme oxygenase-1 alters iron homeostasis in nonerythroid cells
    Cheng Li
    Centre for Vascular Research, School of Medical Sciences Pathology and Bosch Institute, University of Sydney, Sydney, NSW 2006, Australia
    Free Radic Biol Med 53:366-74. 2012
    ..Together, our results reveal a novel and coordinated adaptive response of nonerythroid cells to sustained HO-1 induction that has an impact on cellular iron homeostasis...
  16. ncbi Measurements of redox control of nitric oxide bioavailability
    Annong Huang
    Evans Memorial Department of Medicine, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    Methods Enzymol 359:209-16. 2002
    ..Used in combination, these assays can provide considerable insight into the effect of cellular redox status on NO bioactivity and provide the investigator with a good starting point for further mechanistic studies...
  17. ncbi Beyond LDL oxidation: ROS in vascular signal transduction
    Kai Chen
    Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA 02118, USA
    Free Radic Biol Med 35:117-32. 2003
    ..In this review, the data linking ROS to cell signaling is discussed and the notion that ROS mediate a vascular "injury" response is proposed...
  18. ncbi Regulation of angiogenesis by glycogen synthase kinase-3beta
    Hyo Soo Kim
    Whitaker Cardiovascular Institute, Boston University School of Medicine, Massachusetts 02118, USA
    J Biol Chem 277:41888-96. 2002
    ..These data suggest that GSK3beta functions at the nodal point of converging signaling pathways in EC to regulate vessel growth through its control of vascular cell migration and survival...
  19. ncbi Molecules in focus: indoleamine 2,3-dioxygenase
    Nicholas J C King
    Department of Pathology, Bosch Institute, School of Medical Sciences, University of Sydney, Sydney, Australia
    Int J Biochem Cell Biol 39:2167-72. 2007
    ..In this review, we briefly outline the biochemical properties of IDO, its known and hypothetical functions and the medical implications for inhibition or induction of IDO and/or its downstream catabolites in health and disease...
  20. ncbi Suppression of the JNK pathway by induction of a metabolic stress response prevents vascular injury and dysfunction
    Eberhard Schulz
    Department of Cardiology, 2nd Medical Clinic of the University Hospital Mainz, Johannes Gutenberg University, Mainz, Germany
    Circulation 118:1347-57. 2008
    ..Oxidative injury and dysfunction of the vascular endothelium are early and causal features of many vascular diseases. Single antioxidant strategies to prevent vascular injury have met with mixed results...
  21. ncbi Determination of the nature of the heme environment in nitrosyl indoleamine 2,3-dioxygenase using Multiple-scattering analyses of X-ray absorption fine structure
    Jade B Aitken
    Centre for Structural Biology and Structural Chemistry, and Centre for Heavy Metals Research, School of Chemistry, The University of Sydney, New South Wales 2006, Australia
    Biochemistry 43:4892-8. 2004
    ..The results indicate that both the blocking of the heme site to O(2) binding and conformational changes induced by breaking the Fe-N(epsilon) bond may be important mechanisms by which NO inhibits IDO in vitro and in vivo...
  22. ncbi The heme environment of recombinant human indoleamine 2,3-dioxygenase. Structural properties and substrate-ligand interactions
    Andrew C Terentis
    Biochemistry Group, The Heart Research Institute, 145 Missenden Road, Camperdown, New South Wales 2050, Australia
    J Biol Chem 277:15788-94. 2002
    ..Together these data indicate that the strong proximal Fe-His bond and the strong H-bonding and/or steric interactions between l-Trp and dioxygen in the distal pocket are likely crucial for the enzymatic activity of hIDO...
  23. ncbi Vitamin E oxidation in human atherosclerotic lesions
    Andrew C Terentis
    Biochemistry Group, The Heart Research Institute, Camperdown, New South Wales, Australia
    Circ Res 90:333-9. 2002
    ..This study may have important implications regarding antioxidant supplements aimed at preventing LDL oxidation and hence atherogenesis...