S Orrenius

Summary

Affiliation: Karolinska Institutet
Country: Sweden

Publications

  1. ncbi 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
  2. ncbi Review: nuclear events in apoptosis
    J D Robertson
    Division of Toxicology, Institute of Environmental Medicine, Stockholm, SE 171 77, Sweden
    J Struct Biol 129:346-58. 2000
  3. ncbi 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
  4. ncbi Distinct pathways for stimulation of cytochrome c release by etoposide
    J D Robertson
    Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Box 210, SE 171 77 Stockholm, Sweden
    J Biol Chem 275:32438-43. 2000
  5. ncbi Ca2+ homeostasis and cytotoxicity in isolated hepatocytes: studies with extracellular adenosine 5'-triphosphate
    F Mirabelli
    Department of Toxicology, Karolinska Institutet, Stockholm, Sweden
    J Biochem Toxicol 1:29-39. 1986
  6. ncbi Induction of apoptosis and potentiation of TNF- and Fas-mediated apoptosis in U937 cells by the xanthogenate compound D609
    M I Pörn-Ares
    Division of Toxicology, Karolinska Institutet, Stockholm, 17177, Sweden
    Exp Cell Res 235:48-54. 1997
  7. doi An increase in intracellular Ca2+ is required for the activation of mitochondrial calpain to release AIF during cell death
    E Norberg
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Stockholm, Sweden
    Cell Death Differ 15:1857-64. 2008
  8. ncbi Ca2(+)-mobilizing hormones stimulate Ca2+ efflux from hepatocytes
    S K Duddy
    Department of Toxicology, Karolinska Institutet, Stockholm, Sweden
    J Biol Chem 264:20863-6. 1989
  9. ncbi The role of calcium in pre- and postmitochondrial events in tributyltin-induced T-cell apoptosis
    H Stridh
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Stockholm, Sweden
    Biochem Biophys Res Commun 266:460-5. 1999
  10. pmc Hsp27 protects mitochondria of thermotolerant cells against apoptotic stimuli
    A Samali
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
    Cell Stress Chaperones 6:49-58. 2001

Collaborators

Detail Information

Publications88

  1. ncbi 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...
  2. ncbi Review: nuclear events in apoptosis
    J D Robertson
    Division of Toxicology, Institute of Environmental Medicine, Stockholm, SE 171 77, Sweden
    J Struct Biol 129:346-58. 2000
    ....
  3. ncbi 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...
  4. ncbi Distinct pathways for stimulation of cytochrome c release by etoposide
    J D Robertson
    Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Box 210, SE 171 77 Stockholm, Sweden
    J Biol Chem 275:32438-43. 2000
    ....
  5. ncbi Ca2+ homeostasis and cytotoxicity in isolated hepatocytes: studies with extracellular adenosine 5'-triphosphate
    F Mirabelli
    Department of Toxicology, Karolinska Institutet, Stockholm, Sweden
    J Biochem Toxicol 1:29-39. 1986
    ....
  6. ncbi Induction of apoptosis and potentiation of TNF- and Fas-mediated apoptosis in U937 cells by the xanthogenate compound D609
    M I Pörn-Ares
    Division of Toxicology, Karolinska Institutet, Stockholm, 17177, Sweden
    Exp Cell Res 235:48-54. 1997
    ..In summary, the present results show that D609 stimulates SMase activity, potentiates TNF- and Fas-induced apoptosis, and induces apoptosis on its own in U937 cells...
  7. doi An increase in intracellular Ca2+ is required for the activation of mitochondrial calpain to release AIF during cell death
    E Norberg
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Stockholm, Sweden
    Cell Death Differ 15:1857-64. 2008
    ..Inhibition of calpain, or chelation of Ca(2+), but not the suppression of caspase activity, prevented processing and release of AIF. Combined, these results provide novel insights into the mechanism of AIF release during cell death...
  8. ncbi Ca2(+)-mobilizing hormones stimulate Ca2+ efflux from hepatocytes
    S K Duddy
    Department of Toxicology, Karolinska Institutet, Stockholm, Sweden
    J Biol Chem 264:20863-6. 1989
    ....
  9. ncbi The role of calcium in pre- and postmitochondrial events in tributyltin-induced T-cell apoptosis
    H Stridh
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Stockholm, Sweden
    Biochem Biophys Res Commun 266:460-5. 1999
    ..However, the rise in [Ca(2+)](i) is a prerequisite for postmitochondrial events involved in caspase activation prior to the induction of apoptosis...
  10. pmc Hsp27 protects mitochondria of thermotolerant cells against apoptotic stimuli
    A Samali
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
    Cell Stress Chaperones 6:49-58. 2001
    ..A model is presented for the inhibition of apoptosis during thermotolerance in which Hsp27 preferentially blocks mitochondrial cytochrome c release, whereas Hsp72 interferes with apoptosomal caspase activation...
  11. ncbi Role of mitochondria in neuronal apoptosis
    A M Gorman
    Division of Toxicology and Neurotoxicology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
    Dev Neurosci 22:348-58. 2000
    ..Alterations in energy (ATP) production by mitochondria (due to hypoxia or mutations in genes encoding mitochondrial proteins of the electron transport chain) can induce apoptosis in neurons or increase their sensitivity to apoptosis...
  12. ncbi Cleavage of the calpain inhibitor, calpastatin, during apoptosis
    M I Pörn-Ares
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
    Cell Death Differ 5:1028-33. 1998
    ..In conclusion, the results of the present study suggest that caspases may cleave calpastatin and thus, regulate calpain activity during apoptotic cell death...
  13. ncbi DNA damage induces two distinct modes of cell death in ovarian carcinomas
    H Vakifahmetoglu
    Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
    Cell Death Differ 15:555-66. 2008
    ..Thus, we hypothesize that the final mode of cell death triggered by DNA damage in ovarian carcinoma cells is determined by the profile of proteins involved in the regulation of the cell cycle, such as p53- and Chk2-related proteins...
  14. pmc Presence of a pre-apoptotic complex of pro-caspase-3, Hsp60 and Hsp10 in the mitochondrial fraction of jurkat cells
    A Samali
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Box 210, S 171 77, Stockholm, Sweden
    EMBO J 18:2040-8. 1999
    ..This finding suggests that the release of mitochondrial Hsps may also accelerate caspase activation in the cytoplasm of intact cells...
  15. ncbi Caspase involvement in the induction of apoptosis by the environmental toxicants tributyltin and triphenyltin
    H Stridh
    Division of Toxicology, Karolinska Institutet, Stockholm, S 171 77, Sweden
    Toxicol Appl Pharmacol 156:141-6. 1999
    ....
  16. ncbi NK cell-induced cytotoxicity is dependent on a Ca2+ increase in the target
    D J McConkey
    Department of Toxicology, Karolinska Institutet, Stockholm, Sweden
    FASEB J 4:2661-4. 1990
    ..Thus, it is concluded that NK cell killing depends on a Ca2+ increase and appears to involve endogenous endonuclease activation in target cells...
  17. ncbi Involvement of extracellular calcium in phosphatidylserine exposure during apoptosis
    M B Hampton
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Stockholm, Sweden
    FEBS Lett 399:277-82. 1996
    ..We conclude that while an elevation of intracellular Ca2+ is an ineffective trigger of apoptosis in the cells investigated, extracellular Ca2+ is required for efficient PS exposure during apoptosis...
  18. ncbi Protease activation in apoptosis induced by MAL
    C Kohler
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Stockholm, S 171 77, Sweden
    Exp Cell Res 249:260-8. 1999
    ....
  19. ncbi Thermotolerance and cell death are distinct cellular responses to stress: dependence on heat shock proteins
    A Samali
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Box 210, S 171 77, Stockholm, Sweden
    FEBS Lett 461:306-10. 1999
    ..Furthermore, accumulation of Hsps after incubation at 42 degrees C rendered the cells resistant to apoptosis. These results suggest that lack of Hsp induction is the cause rather than the consequence of cell death...
  20. ncbi Apoptosis: a basic biological phenomenon with wide-ranging implications in human disease
    B Fadeel
    Division of Molecular Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
    J Intern Med 258:479-517. 2005
    ..An increased understanding of the signalling pathways that govern the execution of apoptosis and the subsequent clearance of dying cells may thus yield novel targets for therapeutic intervention in a wide range of human maladies...
  21. ncbi Correlation between cytosolic Ca2+ concentration and cytotoxicity in hepatocytes exposed to oxidative stress
    P Nicotera
    Department of Toxicology, Karolinska Institutet, Stockholm, Sweden
    Toxicology 52:55-63. 1988
    ..Our findings provide further support for the hypothesis that a perturbation of intracellular Ca2+ homeostasis is an early and critical event in the development of toxicity in hepatocytes exposed to oxidative stress...
  22. ncbi Dual regulation of caspase activity by hydrogen peroxide: implications for apoptosis
    M B Hampton
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Stockholm, Sweden
    FEBS Lett 414:552-6. 1997
    ..We discuss the physiological implications of cells having to maintain a reducing environment during apoptosis to allow the caspases to function...
  23. ncbi Organotin-induced caspase activation and apoptosis in human peripheral blood lymphocytes
    H Stridh
    Institute of Environmental Medicine, Department of Medicine, Division of Respiratory Medicine, Karolinska Institutet, Stockholm, Sweden
    Chem Res Toxicol 14:791-8. 2001
    ..Taken together, these data suggest that TBT-induced deletion of peripheral lymphocytes is likely to be a component in the overall risk for immunotoxic responses in exposed humans...
  24. ncbi 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...
  25. ncbi 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...
  26. ncbi Current concepts in cell death
    B Zhivotovsky
    Karolinska Institutet, Stockholm, Sweden
    Curr Protoc Cell Biol . 2001
    ..Specific topics pertaining to cell death include structural changes, macromolecular degradation, cellular signaling, the role of mitochondria, and genetic modulation of apoptotic cell death...
  27. ncbi Molecular mechanisms of apoptosis induced by cytotoxic chemicals
    J D Robertson
    Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
    Crit Rev Toxicol 30:609-27. 2000
    ..Finally, we conclude with a critical discussion of the current knowledge in this area and provide recommendations for future directions...
  28. ncbi All along the watchtower: on the regulation of apoptosis regulators
    B Fadeel
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, 171 77 Stockholm, Sweden
    FASEB J 13:1647-57. 1999
    ..We discuss how the regulation of these apoptosis regulators may control the ultimate fate of the cell...
  29. ncbi Cytochrome c release occurs via Ca2+-dependent and Ca2+-independent mechanisms that are regulated by Bax
    V Gogvadze
    Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Box 210, SE-171 77 Stockholm, Sweden
    J Biol Chem 276:19066-71. 2001
    ..Finally, oligomeric Bax appears to be capable of stimulating cytochrome c release via both Ca(2+)-dependent and Ca(2+)-independent mechanisms...
  30. ncbi Radical scavenging compound J 811 inhibits hydrogen peroxide-induced death of cerebellar granule cells
    M E Götz
    Karolinska Institutet, Institute of Environmental Medicine, Stockholm, Sweden
    J Neurosci Res 56:420-6. 1999
    ..Thus the scavestrogen J 811 is a powerful antioxidant able to interfere with radical-mediated cell death and is potentially useful in diseases where reactive oxygen species are involved...
  31. pmc Caspase-2 promotes cytoskeleton protein degradation during apoptotic cell death
    H Vakifahmetoglu-Norberg
    Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm 171 77, Sweden
    Cell Death Dis 4:e940. 2013
    ..Taken together, our results depict a new role for caspase-2 in the regulation of the level of cytoskeleton proteins during apoptosis. ..
  32. doi Cell cycle and cell death in disease: past, present and future
    B Zhivotovsky
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institute, Stockholm, Sweden
    J Intern Med 268:395-409. 2010
    ....
  33. doi Mitochondrial targeting of tBid/Bax: a role for the TOM complex?
    M Ott
    Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
    Cell Death Differ 16:1075-82. 2009
    ..Here, we review recent work on the mechanisms of activation and the targeting of Bax to the mitochondria and discuss the advantages and limitations of the methods used to study this process...
  34. ncbi The most unkindest cut of all: on the multiple roles of mammalian caspases
    B Fadeel
    Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
    Leukemia 14:1514-25. 2000
    ..The present review aims to discuss the multiple roles of the mammalian caspases with particular emphasis on their activation and regulation in cells of leukemic origin and the attendant possibilities of therapeutic intervention...
  35. ncbi Release of adenylate kinase 2 from the mitochondrial intermembrane space during apoptosis
    C Kohler
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Stockholm, Sweden
    FEBS Lett 447:10-2. 1999
    ..Thus, our data suggest that only intermembrane proteins are released from mitochondria during the early phase of the apoptotic process...
  36. ncbi [Apoptosis required for maintenance of homeostasis: familial hemophagocytic lymphohistiocytosis caused by too little cell death]
    B Fadeel
    Institutet för miljömedicin, forskar AT läkare, Karolinska sjukhuset, Stockholm
    Lakartidningen 97:1395-400, 1402. 2000
    ....
  37. ncbi 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...
  38. 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...
  39. ncbi 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...
  40. ncbi 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...
  41. ncbi 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...
  42. pmc Constitutive nuclear NF kappa B/rel DNA-binding activity of rat thymocytes is increased by stimuli that promote apoptosis, but not inhibited by pyrrolidine dithiocarbamate
    A F Slater
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
    Biochem J 312:833-8. 1995
    ..Dithiocarbamates therefore do not exert their anti-apoptotic activity in thymocytes by inhibiting the activation of this transcription factor...
  43. ncbi 2,5-Di(tert-butyl)-1,4-benzohydroquinone--a novel mobilizer of the inositol 1,4,5-trisphosphate-sensitive Ca2+ pool
    G A Moore
    Department of Toxicology, Karolinska Institute, Stockholm, Sweden
    Free Radic Res Commun 8:337-45. 1990
    ..abstract truncated at 250 words)..
  44. ncbi Detection of pro-caspase-3 in cytosol and mitochondria of various tissues
    A Samali
    Institute of Environmental Medicine, Division of Toxicology, Karolinska Institutet, Stockholm, Sweden
    FEBS Lett 431:167-9. 1998
    ..e. tissues in which spontaneous apoptosis plays an important role. Our findings provide further support for mitochondrial localization of pro-caspase-3 and the critical role of this organelle in apoptosis...
  45. ncbi Functional connection between p53 and caspase-2 is essential for apoptosis induced by DNA damage
    H Vakifahmetoglu
    Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
    Oncogene 25:5683-92. 2006
    ..As suppression of caspase-2 expression in 5-FU-treated cells also affects the level of the p53 protein, possibilities of a reciprocal interaction between these proteins are discussed...
  46. ncbi 'Centennial' Nobel Conference on apoptosis and human disease
    J D Robertson
    Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, SE 171 77 Stockholm, Sweden
    Cell Death Differ 9:468-75. 2002
  47. ncbi 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...
  48. ncbi 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...
  49. ncbi 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
    ....
  50. ncbi 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...
  51. ncbi 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...
  52. ncbi 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...
  53. ncbi 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
    ....
  54. ncbi 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...
  55. ncbi Role of cardiolipin in cytochrome c release from mitochondria
    M Ott
    Institute of Environmental Medicine, Karolinska Institutet, Box 210, S 171 77 Stockholm, Sweden
    Cell Death Differ 14:1243-7. 2007
  56. ncbi Assessment of apoptosis and necrosis by DNA fragmentation and morphological criteria
    B Zhivotosky
    Karolinska Institute, Stockholm, Sweden
    Curr Protoc Cell Biol . 2001
    ..A protocol is also provided for Cytospin preparations from cell suspensions...
  57. ncbi 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...
  58. ncbi 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...
  59. doi 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...
  60. doi Analysis of mitochondrial dysfunction during cell death
    Vladimir Gogvadze
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
    Curr Protoc Cell Biol . 2003
    ....
  61. ncbi 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...
  62. ncbi 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...
  63. ncbi 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...
  64. 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...
  65. ncbi 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...
  66. ncbi Familial hemophagocytic lymphohistiocytosis: too little cell death can seriously damage your health
    B Fadeel
    Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Childhood Cancer Research Unit, Astrid Lindgren Children s Hospital, Karolinska Hospital, Stockholm, Sweden
    Leuk Lymphoma 42:13-20. 2001
    ..These observations represent an important step in our understanding of the pathogenesis of FHL and also serve to emphasize the pivotal role of cellular (perforin-based) cytotoxicity in the regulation of immune homeostasis...
  67. ncbi Neural stem cells and cell death
    S Ceccatelli
    Division of Toxicology and Neurotoxicology, Institute of Environmental Medicine, Karolinska Institutet, Box 210, Stockholm S 171 77, Sweden
    Toxicol Lett 149:59-66. 2004
    ..The Fas-induced ERK phosphorylation that we detect in C17.2 cells suggests that in NSC Fas may function as a mediator of growth rather than death...
  68. doi 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...
  69. ncbi 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)...
  70. doi 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...
  71. doi 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
    ....
  72. ncbi 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...
  73. ncbi 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...
  74. ncbi 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...
  75. doi 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
    ....
  76. ncbi [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
  77. ncbi 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...
  78. 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...
  79. ncbi 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
  80. ncbi 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
  81. ncbi 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...
  82. ncbi 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...
  83. ncbi Cardiolipin oxidation sets cytochrome c free
    Sten Orrenius
    Nat Chem Biol 1:188-9. 2005
  84. ncbi 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
  85. ncbi Phosphatidylserine externalization in cardiolipin-deficient cells
    Bengt Fadeel
    Blood 104:1582-3; author reply 1583-4. 2004
  86. ncbi 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
    ....
  87. ncbi 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
    ....
  88. ncbi 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...