W T Dauer

Summary

Affiliation: Columbia University
Country: USA

Publications

  1. ncbi request reprint The ons and offs of inducible transgenic technology: a review
    A Yamamoto
    Department of Pharmacology, Columbia University, New York, New York 10032, USA
    Neurobiol Dis 8:923-32. 2001
  2. pmc Resistance of alpha -synuclein null mice to the parkinsonian neurotoxin MPTP
    William Dauer
    Department of Neurology, Columbia University, New York, NY 10027, USA
    Proc Natl Acad Sci U S A 99:14524-9. 2002
  3. ncbi request reprint Neurotrophic factors and Parkinson's disease: the emergence of a new player?
    William Dauer
    Departments of Neurology and Pharmacology, Columbia University, Neurological Institute of New York, Box 204, 710 West 168th Street, New York, NY 10032, USA
    Sci STKE 2007:pe60. 2007
  4. pmc alpha-Synuclein produces a long-lasting increase in neurotransmitter release
    Shumin Liu
    Department of Pathology, Columbia University, New York, NY, USA
    EMBO J 23:4506-16. 2004
  5. ncbi request reprint Regulation of the development of mesencephalic dopaminergic systems by the selective expression of glial cell line-derived neurotrophic factor in their targets
    Nikolai Kholodilov
    Department of Neurology, Psychiatry, Pharmacology, and Pathology, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA
    J Neurosci 24:3136-46. 2004
  6. pmc Dopamine-modified alpha-synuclein blocks chaperone-mediated autophagy
    Marta Martinez-Vicente
    Department of Anatomy and Structural Biology, Albert Einstein College of Medicine, Yeshiva University, New York, New York 10461, USA
    J Clin Invest 118:777-88. 2008
  7. ncbi request reprint Alpha-synuclein involvement in hippocampal synaptic plasticity: role of NO, cGMP, cGK and CaMKII
    Shumin Liu
    Department of Pathology, Taub Institute, Columbia University, New York, NY 10032, USA
    Eur J Neurosci 25:3583-96. 2007
  8. ncbi request reprint Parkinson's disease: mechanisms and models
    William Dauer
    Department of Neurology, Columbia University, New York, NY 10032, USA
    Neuron 39:889-909. 2003
  9. ncbi request reprint Mouse models of torsinA dysfunction
    William Dauer
    Departments of Neurology and Pharmacology, Columbia University, New York, New York, USA
    Adv Neurol 94:67-72. 2004
  10. pmc The kinase domain of mitochondrial PINK1 faces the cytoplasm
    Chun Zhou
    Department of Neurology, Columbia University, 650 West 168th Street, New York, NY 10032, USA
    Proc Natl Acad Sci U S A 105:12022-7. 2008

Research Grants

Collaborators

Detail Information

Publications17

  1. ncbi request reprint The ons and offs of inducible transgenic technology: a review
    A Yamamoto
    Department of Pharmacology, Columbia University, New York, New York 10032, USA
    Neurobiol Dis 8:923-32. 2001
    ..These regulatable systems are a new and powerful tool for the neurobiologist and allow one to address a new set of important questions in an in vivo setting...
  2. pmc Resistance of alpha -synuclein null mice to the parkinsonian neurotoxin MPTP
    William Dauer
    Department of Neurology, Columbia University, New York, NY 10027, USA
    Proc Natl Acad Sci U S A 99:14524-9. 2002
    ....
  3. ncbi request reprint Neurotrophic factors and Parkinson's disease: the emergence of a new player?
    William Dauer
    Departments of Neurology and Pharmacology, Columbia University, Neurological Institute of New York, Box 204, 710 West 168th Street, New York, NY 10032, USA
    Sci STKE 2007:pe60. 2007
    ....
  4. pmc alpha-Synuclein produces a long-lasting increase in neurotransmitter release
    Shumin Liu
    Department of Pathology, Columbia University, New York, NY, USA
    EMBO J 23:4506-16. 2004
    ..Thus, alpha-synuclein is involved in synaptic plasticity by augmenting transmitter release from the presynaptic terminal...
  5. ncbi request reprint Regulation of the development of mesencephalic dopaminergic systems by the selective expression of glial cell line-derived neurotrophic factor in their targets
    Nikolai Kholodilov
    Department of Neurology, Psychiatry, Pharmacology, and Pathology, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA
    J Neurosci 24:3136-46. 2004
    ..GDNF in VTA targets, however, is sufficient to regulate the adult number of DA neurons...
  6. pmc Dopamine-modified alpha-synuclein blocks chaperone-mediated autophagy
    Marta Martinez-Vicente
    Department of Anatomy and Structural Biology, Albert Einstein College of Medicine, Yeshiva University, New York, New York 10461, USA
    J Clin Invest 118:777-88. 2008
    ..As blockage of CMA increases cellular vulnerability to stressors, we propose that dopamine-induced autophagic inhibition could explain the selective degeneration of PD dopaminergic neurons...
  7. ncbi request reprint Alpha-synuclein involvement in hippocampal synaptic plasticity: role of NO, cGMP, cGK and CaMKII
    Shumin Liu
    Department of Pathology, Taub Institute, Columbia University, New York, NY 10032, USA
    Eur J Neurosci 25:3583-96. 2007
    ..Thus, our results suggest that NO, cGMP, GMP-dependent protein kinase and calmodulin-dependent protein kinase II play a key role in the redistribution of alpha-synuclein during plasticity...
  8. ncbi request reprint Parkinson's disease: mechanisms and models
    William Dauer
    Department of Neurology, Columbia University, New York, NY 10032, USA
    Neuron 39:889-909. 2003
    ..PD models based on the manipulation of PD genes should prove valuable in elucidating important aspects of the disease, such as selective vulnerability of substantia nigra dopaminergic neurons to the degenerative process...
  9. ncbi request reprint Mouse models of torsinA dysfunction
    William Dauer
    Departments of Neurology and Pharmacology, Columbia University, New York, New York, USA
    Adv Neurol 94:67-72. 2004
  10. pmc The kinase domain of mitochondrial PINK1 faces the cytoplasm
    Chun Zhou
    Department of Neurology, Columbia University, 650 West 168th Street, New York, NY 10032, USA
    Proc Natl Acad Sci U S A 105:12022-7. 2008
    ..These results are critical in rectifying the location and orientation of PINK1 in mitochondria, and they should help decipher its normal physiological function and potential pathogenic role in PD...
  11. doi request reprint The biology and pathology of the familial Parkinson's disease protein LRRK2
    William Dauer
    Department of Neurology, Columbia University, New York, New York, USA
    Mov Disord 25:S40-3. 2010
    ..This review will summarize current knowledge of the clinical and cell biological features of LRRK2, the most common inherited cause of Parkinsonism...
  12. ncbi request reprint Loss of the dystonia-associated protein torsinA selectively disrupts the neuronal nuclear envelope
    Rose E Goodchild
    Department of Neurology, Columbia University, New York, New York 10032, USA
    Neuron 48:923-32. 2005
    ..These observations demonstrate that neurons have a unique requirement for nuclear envelope localized torsinA function and suggest that loss of this activity is a key molecular event in the pathogenesis of DYT1 dystonia...
  13. 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...
  14. 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...
  15. 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...
  16. pmc Thymidine kinase 2 (H126N) knockin mice show the essential role of balanced deoxynucleotide pools for mitochondrial DNA maintenance
    Hasan O Akman
    Department of Neurology, Columbia University Medical Center, New York, NY 10032, USA
    Hum Mol Genet 17:2433-40. 2008
    ..The H126N TK2 mouse is the first knock-in animal model of human MDS and demonstrates that the severity of TK2 deficiency in tissues may determine the organ-specific phenotype...
  17. ncbi request reprint Cortical 5-HT2A receptor signaling modulates anxiety-like behaviors in mice
    Noelia V Weisstaub
    Department of Biology, Columbia University and the New York State Psychiatric Institute, New York, NY 10032, USA
    Science 313:536-40. 2006
    ..These findings indicate a specific role for cortical 5HT2AR function in the modulation of conflict anxiety, consistent with models of cortical, "top-down" influences on risk assessment...

Research Grants3

  1. The mechanism of MPTP resistance in synuclein null mice.
    William Dauer; Fiscal Year: 2007
    ..This proposal exemplifies the type of clinically related fundamental neurobiological research I plan to pursue during my career. ..