L Stefanis

Summary

Affiliation: Columbia University
Country: USA

Publications

  1. ncbi request reprint Induction of CPP32-like activity in PC12 cells by withdrawal of trophic support. Dissociation from apoptosis
    L Stefanis
    Department of Pathology, Taub Center for Alzheimer s Disease Research and Center for Neurobiology and Behavior, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA
    J Biol Chem 271:30663-71. 1996
  2. ncbi request reprint Lack of alpha-synuclein does not alter apoptosis of neonatal catecholaminergic neurons
    Leonidas Stefanis
    Department of Neurology, Columbia University, New York, NY, USA
    Eur J Neurosci 20:1969-72. 2004
  3. ncbi request reprint Synuclein-1 is selectively up-regulated in response to nerve growth factor treatment in PC12 cells
    L Stefanis
    Department of Neurology, Columbia University, New York, USA
    J Neurochem 76:1165-76. 2001
  4. ncbi request reprint Caspase-dependent and -independent neuronal death: two distinct pathways to neuronal injury
    L Stefanis
    Department of Neurology and Pathology, Columbia University, USA
    Neuroscientist 11:50-62. 2005
  5. ncbi request reprint Expression of A53T mutant but not wild-type alpha-synuclein in PC12 cells induces alterations of the ubiquitin-dependent degradation system, loss of dopamine release, and autophagic cell death
    L Stefanis
    Department of Pathology, Columbia University, New York, New York 10032, USA
    J Neurosci 21:9549-60. 2001
  6. ncbi request reprint Proteasomal inhibition leads to formation of ubiquitin/alpha-synuclein-immunoreactive inclusions in PC12 cells
    H J Rideout
    Department of Neurology, Columbia University, New York 10032, USA
    J Neurochem 78:899-908. 2001
  7. ncbi request reprint Application of proteasomal inhibitors to mouse sympathetic neurons activates the intrinsic apoptotic pathway
    Isabelle Lang-Rollin
    Department of Neurology, Columbia University, New York, USA
    J Neurochem 90:1511-20. 2004
  8. ncbi request reprint Inhibitors of trypsin-like serine proteases prevent DNA damage-induced neuronal death by acting upstream of the mitochondrial checkpoint and of p53 induction
    H J Rideout
    Department of Neurology, Columbia University, New York, NY 10032, USA
    Neuroscience 107:339-52. 2001
  9. ncbi request reprint RAIDD is required for apoptosis of PC12 cells and sympathetic neurons induced by trophic factor withdrawal
    Q Wang
    Department of Neurology, Columbia University, New York, USA
    Cell Death Differ 13:75-83. 2006
  10. ncbi request reprint Apoptosis and the conformational change of Bax induced by proteasomal inhibition of PC12 cells are inhibited by bcl-xL and bcl-2
    I Lang-Rollin
    Department of Neurology, Columbia University, New York, NY, USA
    Apoptosis 10:809-20. 2005

Collaborators

Detail Information

Publications34

  1. ncbi request reprint Induction of CPP32-like activity in PC12 cells by withdrawal of trophic support. Dissociation from apoptosis
    L Stefanis
    Department of Pathology, Taub Center for Alzheimer s Disease Research and Center for Neurobiology and Behavior, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA
    J Biol Chem 271:30663-71. 1996
    ....
  2. ncbi request reprint Lack of alpha-synuclein does not alter apoptosis of neonatal catecholaminergic neurons
    Leonidas Stefanis
    Department of Neurology, Columbia University, New York, NY, USA
    Eur J Neurosci 20:1969-72. 2004
    ..Therefore, alpha-synuclein is unlikely to play a significant role in apoptotic signalling in catecholaminergic neurons of the neonatal nervous system...
  3. ncbi request reprint Synuclein-1 is selectively up-regulated in response to nerve growth factor treatment in PC12 cells
    L Stefanis
    Department of Neurology, Columbia University, New York, USA
    J Neurochem 76:1165-76. 2001
    ..In contrast, there is no correlation between synuclein expression and apoptotic death following trophic deprivation...
  4. ncbi request reprint Caspase-dependent and -independent neuronal death: two distinct pathways to neuronal injury
    L Stefanis
    Department of Neurology and Pathology, Columbia University, USA
    Neuroscientist 11:50-62. 2005
    ..In disease states, in which a combination of apoptotic and nonapoptotic death occurs, therapeutic strategies need to take into account both caspase-dependent and -independent pathways...
  5. ncbi request reprint Expression of A53T mutant but not wild-type alpha-synuclein in PC12 cells induces alterations of the ubiquitin-dependent degradation system, loss of dopamine release, and autophagic cell death
    L Stefanis
    Department of Pathology, Columbia University, New York, New York 10032, USA
    J Neurosci 21:9549-60. 2001
    ..These cells may serve as a model to study the effects of aberrant alpha-synuclein on dopaminergic cell function and survival...
  6. ncbi request reprint Proteasomal inhibition leads to formation of ubiquitin/alpha-synuclein-immunoreactive inclusions in PC12 cells
    H J Rideout
    Department of Neurology, Columbia University, New York 10032, USA
    J Neurochem 78:899-908. 2001
    ..Our findings suggest that inclusion body formation and cell death may be dissociated from one another...
  7. ncbi request reprint Application of proteasomal inhibitors to mouse sympathetic neurons activates the intrinsic apoptotic pathway
    Isabelle Lang-Rollin
    Department of Neurology, Columbia University, New York, USA
    J Neurochem 90:1511-20. 2004
    ..We conclude that proteasomal inhibition of mouse sympathetic neurons activates the intrinsic apoptotic pathway involving bcl-2 family members and the mitochondria...
  8. ncbi request reprint Inhibitors of trypsin-like serine proteases prevent DNA damage-induced neuronal death by acting upstream of the mitochondrial checkpoint and of p53 induction
    H J Rideout
    Department of Neurology, Columbia University, New York, NY 10032, USA
    Neuroscience 107:339-52. 2001
    ..We conclude that therapeutic strategies based on serine protease inhibition may be useful in preventing neuronal cell death...
  9. ncbi request reprint RAIDD is required for apoptosis of PC12 cells and sympathetic neurons induced by trophic factor withdrawal
    Q Wang
    Department of Neurology, Columbia University, New York, USA
    Cell Death Differ 13:75-83. 2006
    ..This is the first demonstration of the involvement of RAIDD in apoptosis, and provides further support for the idea that apoptotic pathways in the same system may differ depending on the initiating stimulus...
  10. ncbi request reprint Apoptosis and the conformational change of Bax induced by proteasomal inhibition of PC12 cells are inhibited by bcl-xL and bcl-2
    I Lang-Rollin
    Department of Neurology, Columbia University, New York, NY, USA
    Apoptosis 10:809-20. 2005
    ..Significantly, antiapoptotic bcl-2 family members prevent apoptosis by inhibiting Bax conformational change. Increased levels of Bim may contribute to cell death in this model...
  11. ncbi request reprint Caspase inhibition: a potential therapeutic strategy in neurological diseases
    H J Rideout
    Department of Neurology, Columbia University, New York, NY 10032, USA
    Histol Histopathol 16:895-908. 2001
    ....
  12. ncbi request reprint Lack of p53 delays apoptosis, but increases ubiquitinated inclusions, in proteasomal inhibitor-treated cultured cortical neurons
    Paula Dietrich
    Department of Neurology, Columbia University, Black Building Room 326, 650 W 168 Street, New York, NY 10032, USA
    Mol Cell Neurosci 24:430-41. 2003
    ..We conclude that p53 plays a role in cortical neuron apoptosis induced by proteasomal inhibition and, despite the fact that it localizes to inclusions, it is not necessary for their formation...
  13. ncbi request reprint RAIDD aggregation facilitates apoptotic death of PC12 cells and sympathetic neurons
    O Jabado
    Department of Neurology, Columbia University, USA
    Cell Death Differ 11:618-30. 2004
    ..Therefore, RAIDD aggregation is important for its death-promoting effects and may play a role in trophic factor withdrawal-induced neuronal apoptosis...
  14. ncbi request reprint Involvement of macroautophagy in the dissolution of neuronal inclusions
    Hardy J Rideout
    Department of Neurology, Columbia University, New York, USA
    Int J Biochem Cell Biol 36:2551-62. 2004
    ..These data further support the idea that in this model inclusions and neuronal cell death are independent processes...
  15. ncbi request reprint Ubiquitinated inclusions and neuronal cell death
    I Lang-Rollin
    Department of Neurology, Columbia University, New York, NY 10032, USA
    Histol Histopathol 18:509-17. 2003
    ..The processes of inclusion formation and neuronal cell death share some common mechanisms, but can also be dissociated at a certain level...
  16. ncbi request reprint Delaying caspase activation by Bcl-2: A clue to disease retardation in a transgenic mouse model of amyotrophic lateral sclerosis
    S Vukosavic
    Departments of Neurology and Pathology, Columbia University, New York, New York 10032, USA
    J Neurosci 20:9119-25. 2000
    ....
  17. ncbi request reprint Dopaminergic neurons in rat ventral midbrain cultures undergo selective apoptosis and form inclusions, but do not up-regulate iHSP70, following proteasomal inhibition
    Hardy J Rideout
    Department of Neurology, Columbia University, New York, NY 10032, USA
    J Neurochem 93:1304-13. 2005
    ..This failure may explain in part the increased sensitivity of these neurons to proteasomal inhibitors...
  18. ncbi request reprint Alpha-synuclein overexpression in PC12 and chromaffin cells impairs catecholamine release by interfering with a late step in exocytosis
    Kristin E Larsen
    Department of Neurology, Columbia University School of Medicine, New York, New York 10032, USA
    J Neurosci 26:11915-22. 2006
    ..We conclude that alpha-syn overexpression inhibits a vesicle "priming" step, after secretory vesicle trafficking to "docking" sites but before calcium-dependent vesicle membrane fusion...
  19. doi request reprint A novel cell death pathway that is partially caspase dependent, but morphologically non-apoptotic, elicited by proteasomal inhibition of rat sympathetic neurons
    Isabelle Lang-Rollin
    Department of Neurology, Columbia University, New York, USA
    J Neurochem 105:653-65. 2008
    ..The type of death described herein may be relevant to neurodegenerative diseases, where morphological evidence for apoptosis has been scant...
  20. ncbi request reprint alpha-synuclein is required for the fibrillar nature of ubiquitinated inclusions induced by proteasomal inhibition in primary neurons
    Hardy J Rideout
    Departments of Neurology and Pathology, Columbia University, New York, New York 10032, USA
    J Biol Chem 279:46915-20. 2004
    ..The lack of effect on survival in alpha-synuclein knock-out cultures further suggests that the fibrillar nature of the inclusions does not contribute to neuronal degeneration in this model...
  21. ncbi request reprint Proteasomal inhibition-induced inclusion formation and death in cortical neurons require transcription and ubiquitination
    Hardy J Rideout
    Department of Neurology, Columbia University, New York, New York 10032, USA
    Mol Cell Neurosci 21:223-38. 2002
    ....
  22. ncbi request reprint Regulation of alpha-synuclein by bFGF in cultured ventral midbrain dopaminergic neurons
    Hardy J Rideout
    Department of Neurology, Columbia University, Black Building Room 326, 650 W 168th Street, New York, NY 10032, USA
    J Neurochem 84:803-13. 2003
    ..These results suggest that distinct growth factors may thus mediate plasticity responses or influence disease states in ventral midbrain dopaminergic neurons...
  23. ncbi request reprint Cyclin-dependent kinase activity is required for apoptotic death but not inclusion formation in cortical neurons after proteasomal inhibition
    Hardy J Rideout
    Department of Neurology, Columbia University, New York, New York 10032, USA
    J Neurosci 23:1237-45. 2003
    ..This suggests that there are parallel pathways regulating neuronal death and inclusion formation elicited by proteasomal inhibition in cortical neurons...
  24. ncbi request reprint Alpha-synuclein activation of protein phosphatase 2A reduces tyrosine hydroxylase phosphorylation in dopaminergic cells
    Xiangmin Peng
    Department of Neurology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA
    J Cell Sci 118:3523-30. 2005
    ..Together the data reveal a functional interaction between alpha-synuclein and PP2A that leads to PP2A activation and underscores a key role for alpha-synuclein in protein phosphorylation...
  25. ncbi request reprint Mechanisms of caspase-independent neuronal death: energy depletion and free radical generation
    Isabelle C J Lang-Rollin
    Department of Neurology, Columbia University, New York, New York 10032, USA
    J Neurosci 23:11015-25. 2003
    ..We conclude that energy failure and free radical generation contribute to caspase-independent neuronal death. Both could represent potential targets for therapeutic interventions complementary to caspase inhibition...
  26. ncbi request reprint Mutations in the neurofilament light gene linked to Charcot-Marie-Tooth disease cause defects in transport
    Raul Perez-Olle
    Department of Pathology, Columbia University Medical Center, New York, NY 10032, USA
    J Neurochem 93:861-74. 2005
    ..Our results suggest that these generalized axonal transport defects could be responsible for the neuropathy in Charcot-Marie-Tooth disease...
  27. ncbi request reprint Neurobiology of alpha-synuclein
    Kostas Vekrellis
    Neurobiology Laboratory, Institute of Biomedical Research of the Academy of Athens, Greece, Columbia University, New York, NY
    Mol Neurobiol 30:1-21. 2004
    ..We focus in particular on the fibrilization potential of alpha-synuclein and on its link with defects in protein degradation...
  28. doi request reprint The S18Y polymorphic variant of UCH-L1 confers an antioxidant function to neuronal cells
    Elli Kyratzi
    Division of Basic Neurosciences, Biomedical Research Foundation, Academy of Athens, Athens, Greece
    Hum Mol Genet 17:2160-71. 2008
    ..Our results furthermore provide indirect evidence for the importance of oxidative stress as a pathogenetic factor in certain forms of sporadic PD...
  29. ncbi request reprint A novel pathway for transcriptional regulation of alpha-synuclein
    R Lee Clough
    Division of Basic Neurosciences, Foundation for Biomedical Research of the Academy of Athens IIBEAA, 11527 Athens, Greece
    FASEB J 21:596-607. 2007
    ..Targeting of these pathways may serve to modulate alpha-synuclein so that it achieves desirable levels within neuronal cells...
  30. ncbi request reprint Differential effects of Parkin and its mutants on protein aggregation, the ubiquitin-proteasome system, and neuronal cell death in human neuroblastoma cells
    Elli Kyratzi
    Division of Basic Neurosciences, Foundation for Biomedical Research of the Academy of Athens, Athens, Greece
    J Neurochem 102:1292-303. 2007
    ..This raises a note of caution regarding forced over-expression of Parkin as a neuroprotective strategy in PD or other neurodegenerative conditions and suggests a possible toxic gain of function for certain mutant forms of Parkin...
  31. pmc Wild type alpha-synuclein is degraded by chaperone-mediated autophagy and macroautophagy in neuronal cells
    Tereza Vogiatzi
    Division of Basic Neurosciences, Biomedical Research Foundation of the Academy of Athens, Soranou Efesiou 4, Athens, Greece
    J Biol Chem 283:23542-56. 2008
    ..These results indicate that CMA and macroautophagy are important pathways for WT ASYN degradation in neurons and underline the importance of CMA as degradation machinery in the nervous system...
  32. ncbi request reprint Autophagy and its possible roles in nervous system diseases, damage and repair
    David C Rubinsztein
    Departments of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, Wellcome Trust MRC Building, Addenbrooke s Hospital, Hills Road, Cambridge, UK
    Autophagy 1:11-22. 2005
    ..While many issues remain unresolved, these conditions raise the possibility that autophagy can have either deleterious or protective effects depending on the specific situation and stage in the pathological process...
  33. ncbi request reprint Impaired degradation of mutant alpha-synuclein by chaperone-mediated autophagy
    Ana Maria Cuervo
    Department of Anatomy and Structural Biology, Marion Bessin Liver Research Center, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Science 305:1292-5. 2004
    ..These findings may underlie the toxic gain-of-function by the mutants...
  34. ncbi request reprint alpha-synuclein degradation by autophagic pathways: a potential key to Parkinson's disease pathogenesis
    Maria Xilouri
    Division of Basic Neurosciences, Biomedical Research Foundation of the Academy of Athens, Athens, Greece
    Autophagy 4:917-9. 2008
    ..It is hypothesized that impairment of either of these two pathways, or of more general lysosomal function, may be an initiating factor in alpha-synuclein accumulation and sporadic PD pathogenesis...