V D Nair

Summary

Affiliation: Mount Sinai School of Medicine
Country: USA

Publications

  1. ncbi request reprint Activation of p53 signaling initiates apoptotic death in a cellular model of Parkinson's disease
    V D Nair
    Department of Neurology, Mount Sinai School of Medicine, One Gustave L Levy Place, New York, NY 10029, USA
    Apoptosis 11:955-66. 2006
  2. pmc Involvement of histone demethylase LSD1 in short-time-scale gene expression changes during cell cycle progression in embryonic stem cells
    Venugopalan D Nair
    Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA
    Mol Cell Biol 32:4861-76. 2012
  3. pmc Differential modulation of Akt/glycogen synthase kinase-3beta pathway regulates apoptotic and cytoprotective signaling responses
    Venugopalan D Nair
    Department of Neurology, Mount Sinai School of Medicine, One Gustave L Levy Place, New York, NY 10029, USA
    J Biol Chem 283:15469-78. 2008
  4. ncbi request reprint p53 mediates nontranscriptional cell death in dopaminergic cells in response to proteasome inhibition
    Venugopalan D Nair
    Department of Neurology, Mount Sinai School of Medicine, New York, New York 10029, USA
    J Biol Chem 281:39550-60. 2006
  5. ncbi request reprint Agonist-specific transactivation of phosphoinositide 3-kinase signaling pathway mediated by the dopamine D2 receptor
    Venugopalan D Nair
    Department of Neurology, Mount Sinai School of Medicine, One Gustave L Levy Place, New York, NY 10029, USA
    J Biol Chem 278:47053-61. 2003
  6. ncbi request reprint Molecular cloning, localization and characterization of a 40-kDa catecholamine-regulated protein
    V D Nair
    Departments of Psychiatry and Behavioral Neurosciences, McMaster University, Hamilton, Ontario, Canada
    J Neurochem 76:1142-52. 2001
  7. ncbi request reprint Early single cell bifurcation of pro- and antiapoptotic states during oxidative stress
    Venugopalan D Nair
    Department of Neurology, Mount Sinai School of Medicine, New York, New York 10029, USA
    J Biol Chem 279:27494-501. 2004
  8. pmc Activation of phosphoinositide 3-kinase by D2 receptor prevents apoptosis in dopaminergic cell lines
    Venugopalan D Nair
    Department of Neurology, Mount Sinai School of Medicine, One Gustave L Levy Place, New York, NY 10029, USA
    Biochem J 373:25-32. 2003
  9. ncbi request reprint Cocaine treatment increases expression of a 40 kDa catecholamine-regulated protein in discrete brain regions
    Niki Sharan
    Department of Psychiatry and Behavioural Neurosciences, McMaster University, Hamilton, Ontario, L8N 3Z5, Canada
    Synapse 47:33-44. 2003
  10. ncbi request reprint Modulation of agonist binding to human dopamine receptor subtypes by L-prolyl-L-leucyl-glycinamide and a peptidomimetic analog
    Vaneeta Verma
    Department of Psychiatry and Behavioural Neuroscience, McMaster University, Hamilton, Ontario, Canada
    J Pharmacol Exp Ther 315:1228-36. 2005

Collaborators

Detail Information

Publications10

  1. ncbi request reprint Activation of p53 signaling initiates apoptotic death in a cellular model of Parkinson's disease
    V D Nair
    Department of Neurology, Mount Sinai School of Medicine, One Gustave L Levy Place, New York, NY 10029, USA
    Apoptosis 11:955-66. 2006
    ..Thus, these data suggest that activation of p53 signaling immediately after neurotoxin exposure acts as an initiating factor to mediate apoptosis in dopaminergic cells...
  2. pmc Involvement of histone demethylase LSD1 in short-time-scale gene expression changes during cell cycle progression in embryonic stem cells
    Venugopalan D Nair
    Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA
    Mol Cell Biol 32:4861-76. 2012
    ..Taken together, these results suggest that cell cycle-dependent association and dissociation of LSD1 with chromatin mediates short-time-scale gene expression changes during embryonic stem cell cycle progression...
  3. pmc Differential modulation of Akt/glycogen synthase kinase-3beta pathway regulates apoptotic and cytoprotective signaling responses
    Venugopalan D Nair
    Department of Neurology, Mount Sinai School of Medicine, One Gustave L Levy Place, New York, NY 10029, USA
    J Biol Chem 283:15469-78. 2008
    ..Inhibition of GSK-3beta activity by inhibitor VIII protects cells from H2O2 similar to ropinirole. These results indicate that GSK-3beta downstream of Akt plays a critical role in cell death and survival in these models...
  4. ncbi request reprint p53 mediates nontranscriptional cell death in dopaminergic cells in response to proteasome inhibition
    Venugopalan D Nair
    Department of Neurology, Mount Sinai School of Medicine, New York, New York 10029, USA
    J Biol Chem 281:39550-60. 2006
    ..These results suggest that abnormalities in p53 signaling play a role in dopaminergic cell death induced by proteasome inhibition and may be relevant to neurodegeneration in PD...
  5. ncbi request reprint Agonist-specific transactivation of phosphoinositide 3-kinase signaling pathway mediated by the dopamine D2 receptor
    Venugopalan D Nair
    Department of Neurology, Mount Sinai School of Medicine, One Gustave L Levy Place, New York, NY 10029, USA
    J Biol Chem 278:47053-61. 2003
    ..These results support the hypothesis that specific dopamine agonists stabilize distinct conformations of the D2 receptor that differ in their coupling to G-proteins and to a cytoprotective c-Src/EGFR-mediated PI-3 kinase/Akt pathway...
  6. ncbi request reprint Molecular cloning, localization and characterization of a 40-kDa catecholamine-regulated protein
    V D Nair
    Departments of Psychiatry and Behavioral Neurosciences, McMaster University, Hamilton, Ontario, Canada
    J Neurochem 76:1142-52. 2001
    ..These results suggest that CRP40 could play a protective role against the harmful effects of catecholamine metabolites...
  7. ncbi request reprint Early single cell bifurcation of pro- and antiapoptotic states during oxidative stress
    Venugopalan D Nair
    Department of Neurology, Mount Sinai School of Medicine, New York, New York 10029, USA
    J Biol Chem 279:27494-501. 2004
    ..These studies suggest that the individual cell rapidly and stochastically processes the oxidative stress stimulus, leading to an all-or-none cytoprotective or pro-apoptotic signaling response...
  8. pmc Activation of phosphoinositide 3-kinase by D2 receptor prevents apoptosis in dopaminergic cell lines
    Venugopalan D Nair
    Department of Neurology, Mount Sinai School of Medicine, One Gustave L Levy Place, New York, NY 10029, USA
    Biochem J 373:25-32. 2003
    ..These studies indicate that certain dopamine agonists can complex with D(2) receptors to preferentially transactivate neuroprotective signalling pathways and to mediate increased cell survival...
  9. ncbi request reprint Cocaine treatment increases expression of a 40 kDa catecholamine-regulated protein in discrete brain regions
    Niki Sharan
    Department of Psychiatry and Behavioural Neurosciences, McMaster University, Hamilton, Ontario, L8N 3Z5, Canada
    Synapse 47:33-44. 2003
    ..Elevated levels of CRP40 could play a protective role for dopamine neurons in response to increased oxidative stress that has been shown to be induced by cocaine and that can lead to apoptosis and neurodegeneration...
  10. ncbi request reprint Modulation of agonist binding to human dopamine receptor subtypes by L-prolyl-L-leucyl-glycinamide and a peptidomimetic analog
    Vaneeta Verma
    Department of Psychiatry and Behavioural Neuroscience, McMaster University, Hamilton, Ontario, Canada
    J Pharmacol Exp Ther 315:1228-36. 2005
    ..These results suggest that PLG possibly modulates DA D2S, D2L, and D4 receptors in an allosteric manner and that the coupling of D2 receptors to the G protein is essential for this modulation to occur...