Sten Orrenius

Summary

Affiliation: Karolinska Institutet
Country: Sweden

Publications

  1. ncbi request reprint Mitochondrial oxidative stress: implications for cell death
    Sten Orrenius
    Institute of Environmental Medicine, Karolinska Institutet, S 171 77 Stockholm, Sweden
    Annu Rev Pharmacol Toxicol 47:143-83. 2007
  2. ncbi request reprint Mitochondria, oxidative stress and cell death
    Martin Ott
    Institute of Environmental Medicine, Karolinska Institutet, S 171 77 Stockholm, Sweden
    Apoptosis 12:913-22. 2007
  3. doi request reprint Autophagy in toxicology: cause or consequence?
    Sten Orrenius
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, SE 17177 Stockholm, Sweden
    Annu Rev Pharmacol Toxicol 53:275-97. 2013
  4. ncbi request reprint The future of toxicology--does it matter how cells die?
    Sten Orrenius
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Stockholm, Sweden
    Chem Res Toxicol 19:729-33. 2006
  5. ncbi request reprint Early work on apoptosis, an interview with Sten Orrenius
    Sten Orrenius
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Box 210, SE 171 77 Stockholm, Sweden
    Cell Death Differ 13:1-4. 2006
  6. ncbi request reprint Reactive oxygen species in mitochondria-mediated cell death
    Sten Orrenius
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
    Drug Metab Rev 39:443-55. 2007
  7. doi request reprint Cell death mechanisms and their implications in toxicology
    Sten Orrenius
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Box 210, SE 171 77 Stockholm, Sweden
    Toxicol Sci 119:3-19. 2011
  8. ncbi request reprint Differential regulation of the mitochondrial and death receptor pathways in neural stem cells
    Christoffer Tamm
    Institute of Environmental Medicine, Division of Toxicology and Neurotoxicology, Karolinska Institutet, 71 77 Stockholm, Sweden
    Eur J Neurosci 19:2613-21. 2004
  9. pmc Processed caspase-2 can induce mitochondria-mediated apoptosis independently of its enzymatic activity
    John D Robertson
    Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, 171 77 Stockholm, Sweden
    EMBO Rep 5:643-8. 2004
  10. doi request reprint Analysis of mitochondrial dysfunction during cell death
    Vladimir Gogvadze
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
    Curr Protoc Cell Biol . 2003

Collaborators

Detail Information

Publications55

  1. ncbi request reprint Mitochondrial oxidative stress: implications for cell death
    Sten Orrenius
    Institute of Environmental Medicine, Karolinska Institutet, S 171 77 Stockholm, Sweden
    Annu Rev Pharmacol Toxicol 47:143-83. 2007
    ..Taken together, these findings have placed the mitochondria in the focus of current cell death research...
  2. ncbi request reprint Mitochondria, oxidative stress and cell death
    Martin Ott
    Institute of Environmental Medicine, Karolinska Institutet, S 171 77 Stockholm, Sweden
    Apoptosis 12:913-22. 2007
    ..Conversely, mitochondrial antioxidant enzymes protect from apoptosis. Hence, there is accumulating evidence supporting a direct link between mitochondria, oxidative stress and cell death...
  3. doi request reprint Autophagy in toxicology: cause or consequence?
    Sten Orrenius
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, SE 17177 Stockholm, Sweden
    Annu Rev Pharmacol Toxicol 53:275-97. 2013
    ..However, the relative contribution of autophagy to the overall toxicity of these compounds is not always clear, and further research is needed to clarify the toxicological significance of this process...
  4. ncbi request reprint The future of toxicology--does it matter how cells die?
    Sten Orrenius
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Stockholm, Sweden
    Chem Res Toxicol 19:729-33. 2006
  5. ncbi request reprint Early work on apoptosis, an interview with Sten Orrenius
    Sten Orrenius
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Box 210, SE 171 77 Stockholm, Sweden
    Cell Death Differ 13:1-4. 2006
  6. ncbi request reprint Reactive oxygen species in mitochondria-mediated cell death
    Sten Orrenius
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
    Drug Metab Rev 39:443-55. 2007
    ..Taken together, these findings have placed the mitochondria in the focus of current cell death research...
  7. doi request reprint Cell death mechanisms and their implications in toxicology
    Sten Orrenius
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Box 210, SE 171 77 Stockholm, Sweden
    Toxicol Sci 119:3-19. 2011
    ..Hence, the cell death and phagocytosis regulatory networks offer a multitude of targets for toxic chemicals...
  8. ncbi request reprint Differential regulation of the mitochondrial and death receptor pathways in neural stem cells
    Christoffer Tamm
    Institute of Environmental Medicine, Division of Toxicology and Neurotoxicology, Karolinska Institutet, 71 77 Stockholm, Sweden
    Eur J Neurosci 19:2613-21. 2004
    ..Combined, our findings indicate that while NSCs are sensitive to cytotoxic stimuli that involve an engagement of mitochondria, Fas treatment does not induce death and may have an alternative role...
  9. pmc Processed caspase-2 can induce mitochondria-mediated apoptosis independently of its enzymatic activity
    John D Robertson
    Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, 171 77 Stockholm, Sweden
    EMBO Rep 5:643-8. 2004
    ..Combined, our data suggest that caspase-2 retains a unique ability to engage directly the mitochondrial apoptotic pathway, an effect that requires processing of the zymogen but not the associated catalytic activity...
  10. doi request reprint Analysis of mitochondrial dysfunction during cell death
    Vladimir Gogvadze
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
    Curr Protoc Cell Biol . 2003
    ....
  11. doi request reprint Mitochondria as targets for cancer chemotherapy
    Vladimir Gogvadze
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
    Semin Cancer Biol 19:57-66. 2009
    ..This review is devoted to the role of mitochondria in cell death, and describes how targeting of mitochondria can make tumor cells more susceptible to anticancer treatment...
  12. ncbi request reprint Phosphatidylserine exposure in Fas type I cells is mitochondria-dependent
    Wanlaya Uthaisang
    Institute of Environmental Medicine, Division of Toxicology, Nobels vag 13, Karolinska Institutet, 171 77, Stockholm, Sweden
    FEBS Lett 545:110-4. 2003
    ..These studies thus demonstrate that PS externalization and clearance of cell corpses are mitochondria-dependent events, and show that these events can be dissociated from other features of the apoptotic program, in Fas type I cells...
  13. ncbi request reprint Plasma membrane sequestration of apoptotic protease-activating factor-1 in human B-lymphoma cells: a novel mechanism of chemoresistance
    Yu Sun
    Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
    Blood 105:4070-7. 2005
    ..Together, our findings suggest that ectopic (noncytosolic) localization of Apaf-1 may constitute a novel mechanism of chemoresistance in B lymphoma...
  14. doi request reprint Involvement of Ca2+ and ROS in alpha-tocopheryl succinate-induced mitochondrial permeabilization
    Vladimir Gogvadze
    Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
    Int J Cancer 127:1823-32. 2010
    ..Importantly, Ca(2+)-induced mitochondrial destabilization might cooperate with Bax-mediated mitochondrial outer membrane permeabilization to induce cytochrome c release from mitochondria...
  15. doi request reprint Reactive oxygen species generated in different compartments induce cell death, survival, or senescence
    Emiliano Panieri
    Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, SE 171 77 Stockholm, Sweden
    Free Radic Biol Med 57:176-87. 2013
    ..Combined, our data provide evidence that ROS might dictate different cellular consequences depending on their overall concentration at steady-state levels and on their site of generation...
  16. ncbi request reprint Caspase-2 permeabilizes the outer mitochondrial membrane and disrupts the binding of cytochrome c to anionic phospholipids
    Mari Enoksson
    Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Box 210, SE 171 77 Stockholm, Sweden
    J Biol Chem 279:49575-8. 2004
    ....
  17. ncbi request reprint Cardiolipin is not required for Bax-mediated cytochrome c release from yeast mitochondria
    Suzanne L Iverson
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Box 210, SE 171 77 Stockholm, Sweden
    J Biol Chem 279:1100-7. 2004
    ..In contrast, they support our recently proposed two-step mechanism of cytochrome c release, which suggests that CL is required for binding cytochrome c to the inner mitochondrial membrane...
  18. ncbi request reprint Indirect effects of Bax and Bak initiate the mitochondrial alterations that lead to cytochrome c release during arsenic trioxide-induced apoptosis
    Leta K Nutt
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Stockholm, Sweden
    Cancer Biol Ther 4:459-67. 2005
    ..Furthermore, the results implicate reactive oxygen species in a concentration-dependent mechanistic switch between apoptosis and necrosis...
  19. pmc Critical role for hyperpolarization-activated cyclic nucleotide-gated channel 2 in the AIF-mediated apoptosis
    Erik Norberg
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
    EMBO J 29:3869-78. 2010
    ..Our findings demonstrate a novel role for the HCN2 channel by providing evidence that it can act as an upstream regulator of cell death triggered by PKC inhibitors...
  20. ncbi request reprint Overexpression of glutaredoxin 2 attenuates apoptosis by preventing cytochrome c release
    Mari Enoksson
    Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, SE 171 77 Stockholm, Sweden
    Biochem Biophys Res Commun 327:774-9. 2005
    ..We propose that Grx2 facilitates the maintenance of cellular redox homeostasis upon treatment with apoptotic agents, thereby preventing cardiolipin oxidation and cytochrome c release...
  21. ncbi request reprint Regulation of cell death: the calcium-apoptosis link
    Sten Orrenius
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Box 210, SE 171 77 Stockholm, Sweden
    Nat Rev Mol Cell Biol 4:552-65. 2003
    ..However, more recently it has become clear that cellular Ca2+ overload, or perturbation of intracellular Ca2+ compartmentalization, can cause cytotoxicity and trigger either apoptotic or necrotic cell death...
  22. pmc Mitochondrial cytochrome c release may occur by volume-dependent mechanisms not involving permeability transition
    Vladimir Gogvadze
    Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Box 210, SE 171 77 Stockholm, Sweden
    Biochem J 378:213-7. 2004
    ..In contrast with mitochondrial permeability transition-dependent release of cytochrome c, in the present study mitochondria remain intact and functionally active...
  23. doi request reprint Oxidative modification sensitizes mitochondrial apoptosis-inducing factor to calpain-mediated processing
    Erik Norberg
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, SE 171 77 Stockholm, Sweden
    Free Radic Biol Med 48:791-7. 2010
    ..Combined, our data provide evidence that ROS-mediated, posttranslational modification of AIF is critical for its cleavage by calpain and thus for AIF-mediated cell death...
  24. doi request reprint Citrate kills tumor cells through activation of apical caspases
    Björn Kruspig
    Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Box 210, 171 77 Stockholm, Sweden
    Cell Mol Life Sci 69:4229-37. 2012
    ..Caspase-8 is activated by proximity-induced dimerization, which might be facilitated by citrate through the stabilization of intermolecular interactions between the proteins...
  25. doi request reprint Calcium and cell death mechanisms: a perspective from the cell death community
    Boris Zhivotovsky
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Box 210, SE 171 77 Stockholm, Sweden
    Cell Calcium 50:211-21. 2011
    ..Characteristics, interrelationship and mechanisms involved in Ca(2+) regulation of these cell death modalities are discussed in this review...
  26. ncbi request reprint The mitochondrial TOM complex is required for tBid/Bax-induced cytochrome c release
    Martin Ott
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, SE 171 77 Stockholm, Sweden
    J Biol Chem 282:27633-9. 2007
    ..Here, we show that the protein translocase of the outer mitochondrial membrane is required for Bax insertion and cytochrome c release...
  27. ncbi request reprint Multiple pathways of cytochrome c release from mitochondria in apoptosis
    Vladimir Gogvadze
    Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Box 210, SE 171 77, Stockholm, Sweden
    Biochim Biophys Acta 1757:639-47. 2006
    ..The variety of mechanisms that can lead to outer membrane permeabilization might explain diversities in the response of mitochondria to numerous apoptotic stimuli in different types of cells...
  28. doi request reprint Mitochondria in cancer cells: what is so special about them?
    Vladimir Gogvadze
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Box 210, Stockholm, SE 171 77, Sweden
    Trends Cell Biol 18:165-73. 2008
    ....
  29. doi request reprint Mitochondria as targets for chemotherapy
    Vladimir Gogvadze
    Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
    Apoptosis 14:624-40. 2009
    ..This review is devoted to the role of mitochondria in neurodegeneration and tumor formation, and describes how targeting of mitochondria can be beneficial in the therapy of these diseases, which affect a large human population...
  30. doi request reprint The Warburg effect and mitochondrial stability in cancer cells
    Vladimir Gogvadze
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Box 210, Stockholm SE 17177, Sweden
    Mol Aspects Med 31:60-74. 2010
    ....
  31. ncbi request reprint Caspase-2 acts upstream of mitochondria to promote cytochrome c release during etoposide-induced apoptosis
    John D Robertson
    Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Box 210, SE 171 77 Stockholm, Sweden
    J Biol Chem 277:29803-9. 2002
    ..Taken together, our data indicate that caspase-2 provides an important link between etoposide-induced DNA damage and the engagement of the mitochondrial apoptotic pathway...
  32. doi request reprint Targeting mitochondria by α-tocopheryl succinate kills neuroblastoma cells irrespective of MycN oncogene expression
    Björn Kruspig
    Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
    Cell Mol Life Sci 69:2091-9. 2012
    ..Prevention of mitochondrial Ca(2+) accumulation or chelation of cytosolic Ca(2+) rescued the cells. Thus, targeting mitochondria might be advantageous for the elimination of tumor cells with otherwise dormant apoptotic pathways...
  33. ncbi request reprint Tributyltin causes cytochrome C release from isolated mitochondria by two discrete mechanisms
    Vladimir Gogvadze
    Division of Toxicology, Institute of Environmental Medicine, Stockholm, SE 171 77, Sweden
    Biochem Biophys Res Commun 292:904-8. 2002
    ..Gigliotti, D., Orrenius, S., and Cotgreave, I. A. (1999) Biochem. Biophys. Res. Commun. 266, 460-465)...
  34. doi request reprint Mitochondrial regulation of cell death: processing of apoptosis-inducing factor (AIF)
    Erik Norberg
    Institute of Environmental Medicine, Division of Toxicology Karolinska Institutet, SE 17177 Stockholm, Sweden
    Biochem Biophys Res Commun 396:95-100. 2010
    ..The current knowledge about the molecular mechanisms regulating the processing and release of AIF from the mitochondria will be summarized and discussed in this review...
  35. ncbi request reprint The cardiolipin-cytochrome c interaction and the mitochondrial regulation of apoptosis
    Suzanne L Iverson
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Stockholm, Sweden
    Arch Biochem Biophys 423:37-46. 2004
    ..In this review, we discuss the significance of the disruption of the CL-cytochrome c interaction for cytochrome c release and apoptosis...
  36. ncbi request reprint Role of mitochondria in toxic cell death
    John D Robertson
    Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Box 210, SE 171 77 Stockholm, Sweden
    Toxicology 181:491-6. 2002
    ....
  37. ncbi request reprint Caspase-2 function in response to DNA damage
    Boris Zhivotovsky
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Box 210, SE 171 77 Stockholm, Sweden
    Biochem Biophys Res Commun 331:859-67. 2005
    ..In this review, current knowledge concerning the structure of this protease and its function in cell physiology and cell death, particularly cell death triggered by DNA damage, is summarized and discussed...
  38. ncbi request reprint Buried alive: a novel approach to cancer treatment
    Bengt Fadeel
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Stockholm, Sweden
    FASEB J 18:1-4. 2004
    ..In other words, inducing the expression of "eat me" signals on cancer cells could be a novel approach to "bury alive" these unwanted cells without the untoward effects of chemotherapy-induced apoptosis...
  39. pmc Cytochrome c release from mitochondria proceeds by a two-step process
    Martin Ott
    Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Box 210, SE 171 77 Stockholm, Sweden
    Proc Natl Acad Sci U S A 99:1259-63. 2002
    ..Our results indicate that the release of cytochrome c involves a distinct two-step process that is undermined when either step is compromised...
  40. ncbi request reprint Mitochondrial regulation of apoptotic cell death
    Sten Orrenius
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Box 210, SE 171 77 Stockholm, Sweden
    Toxicol Lett 149:19-23. 2004
    ..Taken together, these findings have placed the mitochondria in the focus of apoptosis research and further underlined the important function of these organelles in cell life and death...
  41. ncbi request reprint Carcinogenesis and apoptosis: paradigms and paradoxes
    Boris Zhivotovsky
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet Box 210, SE 171 77 Stockholm, Sweden
    Carcinogenesis 27:1939-45. 2006
    ..However, the precise role of these genes and their products in cancer development is less clear. Here, we will discuss some of the current paradigms and paradoxes concerning the involvement of apoptotic genes in carcinogenesis...
  42. ncbi request reprint Evaluation of caspase activity in apoptotic cells
    Camilla Köhler
    Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Box 210, SE 171 77 Stockholm, Sweden
    J Immunol Methods 265:97-110. 2002
    ..Each method is described in general terms and the advantages and disadvantages of each technique are discussed...
  43. ncbi request reprint Defects in the apoptotic machinery of cancer cells: role in drug resistance
    Boris Zhivotovsky
    Institute of Environmental Medicine, Karolinska Institutet, Box 210, SE 171 77 Stockholm, Sweden
    Semin Cancer Biol 13:125-34. 2003
    ..Here we review known differences in the apoptotic machinery in cancer cells, and how this knowledge can be used to increase the efficiency of tumor treatment...
  44. ncbi request reprint Resistance of leukemic cells to 2-chlorodeoxyadenosine is due to a lack of calcium-dependent cytochrome c release
    Joya Chandra
    Institute for Environmental Medicine, Division of Toxicology, and Department of Medicine, Karolinska Institutet, Stockholm, Sweden
    Blood 99:655-63. 2002
    ..Taken together, the data indicate that the mechanism of resistance to CdA may be dictated by changes in Ca2+-sensitive mitochondrial events...
  45. doi request reprint Cell death mechanisms: cross-talk and role in disease
    Boris Zhivotovsky
    Institute of Environmental Medicine, Karolinska Institutet, Box 210, SE 171 77 Stockholm, Sweden
    Exp Cell Res 316:1374-83. 2010
    ..In this review we shall discuss the characteristics and cross-talk between various modes of cell death and their role in cell death-related disorders, notably, neurodegenerative disease and cancer...
  46. ncbi request reprint Mitochondrial regulation of apoptotic cell death
    Vladimir Gogvadze
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Box 210, SE 171 77 Stockholm, Sweden
    Chem Biol Interact 163:4-14. 2006
    ..The multiple mechanisms of mitochondrial permeabilization may explain diversities in the response of mitochondria to numerous apoptotic stimuli in different types of cells...
  47. ncbi request reprint Fas-triggered phosphatidylserine exposure is modulated by intracellular ATP
    Bettina Gleiss
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Stockholm, Sweden
    FEBS Lett 519:153-8. 2002
    ..These studies suggest that intracellular ATP levels can modulate the externalization of PS during apoptosis, and implicate the ATP-dependent aminophospholipid translocase in this process...
  48. ncbi request reprint [Sydney Brenner, Robert Horvitz and John Sulston. Winners of the 2002 Nobel Prize in medicine or physiology. Genetic regulation of organ development and programmed cell death]
    Urban Lendahl
    Institutionen för cell och molekylärbiologi, Karolinska Institutet, Stockholm
    Lakartidningen 99:4026-32. 2002
  49. ncbi request reprint Cardiolipin oxidation sets cytochrome c free
    Sten Orrenius
    Nat Chem Biol 1:188-9. 2005
  50. ncbi request reprint Role of mitochondria in toxic oxidative stress
    Marc W Fariss
    Department of Pharmaceutical Sciences, University of Colorado Cancer Center, Denver, CO 80262, USA
    Mol Interv 5:94-111. 2005
    ....
  51. ncbi request reprint A role for oxidative stress in apoptosis: oxidation and externalization of phosphatidylserine is required for macrophage clearance of cells undergoing Fas-mediated apoptosis
    Valerian E Kagan
    Department of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, PA 15260, USA
    J Immunol 169:487-99. 2002
    ..Taken together, our data suggest that the presence of PS-OX in conjunction with nonoxidized PS on the cell surface is an important signal for macrophage clearance of apoptotic cells...
  52. ncbi request reprint Phosphatidylserine externalization in cardiolipin-deficient cells
    Bengt Fadeel
    Blood 104:1582-3; author reply 1583-4. 2004
  53. ncbi request reprint Visualization of the compartmentalization of glutathione and protein-glutathione mixed disulfides in cultured cells
    Therese Söderdahl
    Division of Biochemical Toxicology, Karolinska Institutet, Stockholm Sweden
    FASEB J 17:124-6. 2003
    ..Similar FACS analyses performed in isolated mitochondria presented a considerable variation in GSH content within mitochondria of uniform granularity from the same preparation...
  54. ncbi request reprint Arsenic stimulates release of cytochrome c from isolated mitochondria via induction of mitochondrial permeability transition
    Juanita Bustamante
    Department of Physical Chemistry, School of Pharmacy and Biochemistry, University of Buenos Aires, Junin 956, 1113 Buenos Aires, Argentina
    Toxicol Appl Pharmacol 207:110-6. 2005
    ....
  55. ncbi request reprint HAMLET, protein folding, and tumor cell death
    K Hun Mok
    Trinity College, School of Biochemistry and Immunology, University of Dublin, Dublin 2, Ireland
    Biochem Biophys Res Commun 354:1-7. 2007