Hoau Yan Wang

Summary

Affiliation: City University of New York
Country: USA

Publications

  1. doi request reprint Reducing amyloid-related Alzheimer's disease pathogenesis by a small molecule targeting filamin A
    Hoau Yan Wang
    Department of Physiology, Pharmacology and Neuroscience, City University of New York Medical School, New York, New York 10031, USA
    J Neurosci 32:9773-84. 2012
  2. pmc High-affinity naloxone binding to filamin a prevents mu opioid receptor-Gs coupling underlying opioid tolerance and dependence
    Hoau Yan Wang
    Department of Physiology and Pharmacology, City University of New York Medical School, New York, New York, USA
    PLoS ONE 3:e1554. 2008
  3. doi request reprint Dissociating beta-amyloid from alpha 7 nicotinic acetylcholine receptor by a novel therapeutic agent, S 24795, normalizes alpha 7 nicotinic acetylcholine and NMDA receptor function in Alzheimer's disease brain
    Hoau Yan Wang
    Department of Physiology and Pharmacology, Sophie Davis School of Biomedical Education, City University of New York Medical School, New York, New York 10031, USA
    J Neurosci 29:10961-73. 2009
  4. ncbi request reprint Gbetagamma that interacts with adenylyl cyclase in opioid tolerance originates from a Gs protein
    Hoau Yan Wang
    Department of Physiology and Pharmacology, City University of New York Medical School, 138th Street and Convent Avenue, New York, New York 10031, USA
    J Neurobiol 66:1302-10. 2006
  5. doi request reprint S 24795 limits beta-amyloid-alpha7 nicotinic receptor interaction and reduces Alzheimer's disease-like pathologies
    Hoau Yan Wang
    Department of Physiology and Pharmacology, Sophie Davis School of Biomedical Education, City University of New York Medical School, New York, New York, USA
    Biol Psychiatry 67:522-30. 2010
  6. ncbi request reprint Ultra-low-dose naloxone suppresses opioid tolerance, dependence and associated changes in mu opioid receptor-G protein coupling and Gbetagamma signaling
    H Y Wang
    Department of Physiology and Pharmacology, City University of New York Medical School, 138th Street and Convent Avenue, New York, NY 10031, USA
    Neuroscience 135:247-61. 2005
  7. pmc Repetitive transcranial magnetic stimulation enhances BDNF-TrkB signaling in both brain and lymphocyte
    Hoau Yan Wang
    Department of Physiology, Pharmacology and Neuroscience, Sophie Davis School of Biomedical Education, The City University of New York Medical School, New York, New York 10031, USA
    J Neurosci 31:11044-54. 2011
  8. pmc Naloxone's pentapeptide binding site on filamin A blocks Mu opioid receptor-Gs coupling and CREB activation of acute morphine
    Hoau Yan Wang
    Department of Physiology and Pharmacology, City University of New York Medical School, New York, New York, United States of America
    PLoS ONE 4:e4282. 2009
  9. pmc Prenatal cocaine exposure increases synaptic localization of a neuronal RasGEF, GRASP-1 via hyperphosphorylation of AMPAR anchoring protein, GRIP
    Kalindi Bakshi
    Department of Physiology, Pharmacology and Neuroscience, Sophie Davis School of Biomedical Education, The City University of New York Medical School, New York, New York, United States of America
    PLoS ONE 6:e25019. 2011
  10. ncbi request reprint Cortical plasticity in Alzheimer's disease in humans and rodents
    Fortunato Battaglia
    City University of New York CUNY School of Medicine, Nathan Kline Institute, Orangeburg, New York, USA
    Biol Psychiatry 62:1405-12. 2007

Collaborators

Detail Information

Publications24

  1. doi request reprint Reducing amyloid-related Alzheimer's disease pathogenesis by a small molecule targeting filamin A
    Hoau Yan Wang
    Department of Physiology, Pharmacology and Neuroscience, City University of New York Medical School, New York, New York 10031, USA
    J Neurosci 32:9773-84. 2012
    ..PTI-125's broad spectrum of beneficial effects is demonstrated here in an intracerebroventricular Aβ(42) infusion mouse model of AD and in human postmortem AD brain tissue...
  2. pmc High-affinity naloxone binding to filamin a prevents mu opioid receptor-Gs coupling underlying opioid tolerance and dependence
    Hoau Yan Wang
    Department of Physiology and Pharmacology, City University of New York Medical School, New York, New York, USA
    PLoS ONE 3:e1554. 2008
    ..These results establish filamin A as the target for ultra-low-dose opioid antagonists previously shown to enhance opioid analgesia and to prevent opioid tolerance and dependence...
  3. doi request reprint Dissociating beta-amyloid from alpha 7 nicotinic acetylcholine receptor by a novel therapeutic agent, S 24795, normalizes alpha 7 nicotinic acetylcholine and NMDA receptor function in Alzheimer's disease brain
    Hoau Yan Wang
    Department of Physiology and Pharmacology, Sophie Davis School of Biomedical Education, City University of New York Medical School, New York, New York 10031, USA
    J Neurosci 29:10961-73. 2009
    ..These findings suggest that the Abeta-alpha7nAChR interaction may be an upstream pathogenic event in AD and demonstrate that some recovery of neuronal channel activities may be achieved in AD brains by removing Abeta from alpha7nAChRs...
  4. ncbi request reprint Gbetagamma that interacts with adenylyl cyclase in opioid tolerance originates from a Gs protein
    Hoau Yan Wang
    Department of Physiology and Pharmacology, City University of New York Medical School, 138th Street and Convent Avenue, New York, New York 10031, USA
    J Neurobiol 66:1302-10. 2006
    ....
  5. doi request reprint S 24795 limits beta-amyloid-alpha7 nicotinic receptor interaction and reduces Alzheimer's disease-like pathologies
    Hoau Yan Wang
    Department of Physiology and Pharmacology, Sophie Davis School of Biomedical Education, City University of New York Medical School, New York, New York, USA
    Biol Psychiatry 67:522-30. 2010
    ..The current study assessed whether the novel alpha7nAChR partial agonist 2-(2-(4-bromophenyl)-2-oxoethyl)-1-methyl pyridinium (S 24795) could reduce AD-like pathologies by interfering with Abeta-alpha7nAChR interaction...
  6. ncbi request reprint Ultra-low-dose naloxone suppresses opioid tolerance, dependence and associated changes in mu opioid receptor-G protein coupling and Gbetagamma signaling
    H Y Wang
    Department of Physiology and Pharmacology, City University of New York Medical School, 138th Street and Convent Avenue, New York, NY 10031, USA
    Neuroscience 135:247-61. 2005
    ..These findings provide a molecular mechanism underpinning opioid tolerance and dependence and their attenuation by ultra-low-dose opioid antagonists...
  7. pmc Repetitive transcranial magnetic stimulation enhances BDNF-TrkB signaling in both brain and lymphocyte
    Hoau Yan Wang
    Department of Physiology, Pharmacology and Neuroscience, Sophie Davis School of Biomedical Education, The City University of New York Medical School, New York, New York 10031, USA
    J Neurosci 31:11044-54. 2011
    ..These findings suggest that rTMS to cortex facilitates BDNF-TrkB-NMDAR functioning in both cortex and lymphocytes...
  8. pmc Naloxone's pentapeptide binding site on filamin A blocks Mu opioid receptor-Gs coupling and CREB activation of acute morphine
    Hoau Yan Wang
    Department of Physiology and Pharmacology, City University of New York Medical School, New York, New York, United States of America
    PLoS ONE 4:e4282. 2009
    ....
  9. pmc Prenatal cocaine exposure increases synaptic localization of a neuronal RasGEF, GRASP-1 via hyperphosphorylation of AMPAR anchoring protein, GRIP
    Kalindi Bakshi
    Department of Physiology, Pharmacology and Neuroscience, Sophie Davis School of Biomedical Education, The City University of New York Medical School, New York, New York, United States of America
    PLoS ONE 6:e25019. 2011
    ....
  10. ncbi request reprint Cortical plasticity in Alzheimer's disease in humans and rodents
    Fortunato Battaglia
    City University of New York CUNY School of Medicine, Nathan Kline Institute, Orangeburg, New York, USA
    Biol Psychiatry 62:1405-12. 2007
    ..We then ascertained whether this deficit might be paralleled by functional abnormalities of N-methyl-D-aspartate (NMDAR) glutamate receptors...
  11. pmc Prenatal cocaine reduces AMPA receptor synaptic expression through hyperphosphorylation of the synaptic anchoring protein GRIP
    Kalindi Bakshi
    Department of Physiology, The City University of New York Medical School, New York, New York 10031, USA
    J Neurosci 29:6308-19. 2009
    ..These data support the restoration of AMPAR activation via suppressing excessive PKC-mediated GRIP phosphorylation as a novel therapeutic approach to treat the neurobehavioral consequences of prenatal cocaine...
  12. ncbi request reprint Clozapine protection against gestational cocaine-induced neurochemical abnormalities
    Elena Yablonsky-Alter
    Department of Physiology and Pharmacology, The City University of New York Medical School, 138 Street and Convent Avenue, New York, NY 10031, USA
    J Pharmacol Exp Ther 312:297-302. 2005
    ..Thus clozapine, which is a partial agonist at the NMDA receptor, may be of value in protecting against gestational cocaine-induced adverse effects in the brain...
  13. ncbi request reprint Alpha 7 nicotinic acetylcholine receptors mediate beta-amyloid peptide-induced tau protein phosphorylation
    Hoau Yan Wang
    Department of Physiology and Pharmacology, City University of New York Medical School, New York, New York 10031, USA
    J Biol Chem 278:31547-53. 2003
    ..More importantly, recombinant-activated ERKs and JNK-1 could differentially phosphorylate tau protein in vitro. Thus, the alpha 7nAChR may mediate A beta-induced tau protein phosphorylation via ERKs and JNK-1...
  14. doi request reprint Prenatal cocaine increases dendritic spine density in cortical and subcortical brain regions of the rat
    Maya Frankfurt
    Department of Physiology Pharmacology, City University of New York Medical School at CCNY, New York, NY 10031, USA
    Dev Neurosci 31:71-5. 2009
    ..Moreover, there were no sex differences in any region examined. These results demonstrate that prenatal cocaine exposure increases spine density in many brain regions at postnatal day 21, and this effect is independent of sex...
  15. ncbi request reprint Increased dopamine receptor signaling and dopamine receptor-G protein coupling in denervated striatum
    Guoping Cai
    Department of Physiology and Pharmacology, The City University of New York Medical School, Convent Avenue and 138th Street, New York, NY 10031, USA
    J Pharmacol Exp Ther 302:1105-12. 2002
    ....
  16. pmc Prenatal cocaine exposure uncouples mGluR1 from Homer1 and Gq Proteins
    Kalindi Bakshi
    Departments of Physiology, Pharmacology and Neuroscience, Sophie Davis School of Biomedical Education, The City University of New York Medical School, New York, New York, United States of America
    PLoS ONE 9:e91671. 2014
    ..Hence, blockade of excessive PKC activation may alleviate abnormalities in mGluR1 signaling and restores mGluR1-regulated brain functions in prenatal cocaine-exposed brains. ..
  17. ncbi request reprint Cerebellar diffuse amyloid plaques are derived from dendritic Abeta42 accumulations in Purkinje cells
    Hoau Yan Wang
    Department of Physiology and Pharmacology, The City University of New York Medical School, New York, New York 10031, USA
    Neurobiol Aging 23:213-23. 2002
    ....
  18. doi request reprint Oxycodone plus ultra-low-dose naltrexone attenuates neuropathic pain and associated mu-opioid receptor-Gs coupling
    Tally M Largent-Milnes
    Department of Pharmacology, College of Medicine, University of Arizona, Tucson, Arizona 85724, USA
    J Pain 9:700-13. 2008
    ..The antihyperalgesic and antiallodynic effects of oxycodone plus ultra-low-dose NTX (Oxytrex, Pain Therapeutics, Inc., San Mateo, CA) suggest a promising new treatment for neuropathic pain...
  19. pmc Cocaine exposure during the early postnatal period diminishes medial frontal cortex Gs coupling to dopamine D1-like receptors in adult rat
    Ning Zhao
    Department of Physiology and Pharmacology, SUNY Downstate Medical Center, Brooklyn, NY, United States
    Neurosci Lett 438:159-62. 2008
    ....
  20. ncbi request reprint Cannabinoid-induced tolerance is associated with a CB1 receptor G protein coupling switch that is prevented by ultra-low dose rimonabant
    Jay J Paquette
    Department of Psychology, Queen s University, Kingston, Ontario, Canada
    Behav Pharmacol 18:767-76. 2007
    ..Cannabinoid-induced tolerance is thus associated with a G protein coupling switch from the inhibitory Gi protein to the excitatory Gs protein, an effect which is prevented by the ultra-low dose rimonabant...
  21. ncbi request reprint Altered neuregulin 1-erbB4 signaling contributes to NMDA receptor hypofunction in schizophrenia
    Chang Gyu Hahn
    Cellular and Molecular Neuropathology Program, Center for Neurobiology and Behavior, Department of Psychiatry, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
    Nat Med 12:824-8. 2006
    ..Therefore, these findings suggest that enhanced NRG1 signaling may contribute to NMDA hypofunction in schizophrenia...
  22. ncbi request reprint Astrocytes accumulate A beta 42 and give rise to astrocytic amyloid plaques in Alzheimer disease brains
    Robert G Nagele
    Department of Molecular Biology, University of Medicine and Dentistry of New Jersey SOM, 2 Medical Center Drive, Stratford, NJ 08084, USA
    Brain Res 971:197-209. 2003
    ..Overall, A beta 42 accumulation and the selective lysis of A beta 42-burdened neurons and astrocytes appear to make a major contribution to the observed amyloid plaques in AD brains...
  23. ncbi request reprint Differential physiologic responses of alpha7 nicotinic acetylcholine receptors to beta-amyloid1-40 and beta-amyloid1-42
    Daniel H S Lee
    Biogen Inc, 14 Cambridge Ctr Bio6, 660, Cambridge, Massachusetts 02142, USA
    J Neurobiol 55:25-30. 2003
    ..Our data suggest a clear pharmacological distinction between Abeta(1-40) and Abeta(1-42)...
  24. ncbi request reprint Consistent immunohistochemical detection of intracellular beta-amyloid42 in pyramidal neurons of Alzheimer's disease entorhinal cortex
    Michael R D'Andrea
    Johnson and Johnson Pharmaceutical Research and Development, Spring House, PA 19477, USA
    Neurosci Lett 333:163-6. 2002
    ..Detection of an abundant intracellular Abeta42 in neurons may provide alternate explanations for the origin of dense-core amyloid plaques in AD cortices other than the conventional chronic extracellular Abeta42 deposition hypothesis...