Wanli W Smith

Summary

Affiliation: Johns Hopkins University
Country: USA

Publications

  1. ncbi Phosphorylation of p66Shc and forkhead proteins mediates Abeta toxicity
    Wanli W Smith
    Molecular Neurobiology Unit, Laboratory of Cellular and Molecular Biology, Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
    J Cell Biol 169:331-9. 2005
  2. ncbi Kinase activity of mutant LRRK2 mediates neuronal toxicity
    Wanli W Smith
    Department of Psychiatry, Division of Neurobiology, Johns Hopkins University School of Medicine, CMSC 8 121, 600 North Wolfe Street, Baltimore, Maryland 21287, USA
    Nat Neurosci 9:1231-3. 2006
  3. ncbi Signaling mechanisms underlying Abeta toxicity: potential therapeutic targets for Alzheimer's disease
    Wanli W Smith
    Division of Neurobiology, Department of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    CNS Neurol Disord Drug Targets 5:355-61. 2006
  4. ncbi Leucine-rich repeat kinase 2 (LRRK2) interacts with parkin, and mutant LRRK2 induces neuronal degeneration
    Wanli W Smith
    Department of Psychiatry, Division of Neurobiology, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Proc Natl Acad Sci U S A 102:18676-81. 2005
  5. ncbi ATF3 plays a protective role against toxicity by N-terminal fragment of mutant huntingtin in stable PC12 cell line
    Yideng Liang
    Division of Neurobiology, Department of Psychiatry, The Johns Hopkins University School of Medicine, CMSC 8 121, 600 N Wolfe St, Baltimore, MD 21287, USA
    Brain Res 1286:221-9. 2009
  6. ncbi CHIP regulates leucine-rich repeat kinase-2 ubiquitination, degradation, and toxicity
    Han Seok Ko
    Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Proc Natl Acad Sci U S A 106:2897-902. 2009
  7. ncbi Synphilin-1 attenuates neuronal degeneration in the A53T alpha-synuclein transgenic mouse model
    Wanli W Smith
    Division of Neurobiology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Hum Mol Genet 19:2087-98. 2010
  8. ncbi Parkinson's disease genetic mutations increase cell susceptibility to stress: mutant alpha-synuclein enhances H2O2- and Sin-1-induced cell death
    Haibing Jiang
    Department of Psychiatry, Division of Neurobiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Neurobiol Aging 28:1709-17. 2007
  9. ncbi Depletion of CBP is directly linked with cellular toxicity caused by mutant huntingtin
    Haibing Jiang
    Division of Neurobiology, Department of Psychiatry, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Neurobiol Dis 23:543-51. 2006
  10. ncbi Parkinson's disease-associated mutations in leucine-rich repeat kinase 2 augment kinase activity
    Andrew B West
    Institute for Cell Engineering, Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Proc Natl Acad Sci U S A 102:16842-7. 2005

Research Grants

  1. LRRK2 and cellular pathways of Parkinson's Disease
    Wanli Smith; Fiscal Year: 2007

Collaborators

Detail Information

Publications19

  1. ncbi Phosphorylation of p66Shc and forkhead proteins mediates Abeta toxicity
    Wanli W Smith
    Molecular Neurobiology Unit, Laboratory of Cellular and Molecular Biology, Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
    J Cell Biol 169:331-9. 2005
    ..These findings underscore the potential usefulness of JNK, p66Shc, and forkhead proteins as therapeutic targets for AD...
  2. ncbi Kinase activity of mutant LRRK2 mediates neuronal toxicity
    Wanli W Smith
    Department of Psychiatry, Division of Neurobiology, Johns Hopkins University School of Medicine, CMSC 8 121, 600 North Wolfe Street, Baltimore, Maryland 21287, USA
    Nat Neurosci 9:1231-3. 2006
    ..These data elucidate the pathogenesis of LRRK2-linked Parkinson disease, potentially illuminate mechanisms of sporadic Parkinson disease and suggest therapeutic targets...
  3. ncbi Signaling mechanisms underlying Abeta toxicity: potential therapeutic targets for Alzheimer's disease
    Wanli W Smith
    Division of Neurobiology, Department of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    CNS Neurol Disord Drug Targets 5:355-61. 2006
    ....
  4. ncbi Leucine-rich repeat kinase 2 (LRRK2) interacts with parkin, and mutant LRRK2 induces neuronal degeneration
    Wanli W Smith
    Department of Psychiatry, Division of Neurobiology, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Proc Natl Acad Sci U S A 102:18676-81. 2005
    ....
  5. ncbi ATF3 plays a protective role against toxicity by N-terminal fragment of mutant huntingtin in stable PC12 cell line
    Yideng Liang
    Division of Neurobiology, Department of Psychiatry, The Johns Hopkins University School of Medicine, CMSC 8 121, 600 N Wolfe St, Baltimore, MD 21287, USA
    Brain Res 1286:221-9. 2009
    ..These results indicated that ATF3 plays a critical role in toxicity induced by mutant Htt-N63 and may lead to a useful therapeutic target...
  6. ncbi CHIP regulates leucine-rich repeat kinase-2 ubiquitination, degradation, and toxicity
    Han Seok Ko
    Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Proc Natl Acad Sci U S A 106:2897-902. 2009
    ..Thus, increasing CHIP E3 ligase activity and blocking HSP90 chaperone activity can prevent the deleterious effects of LRRK2. These findings point to potential treatment options for LRRK2-associated PD...
  7. ncbi Synphilin-1 attenuates neuronal degeneration in the A53T alpha-synuclein transgenic mouse model
    Wanli W Smith
    Division of Neurobiology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Hum Mol Genet 19:2087-98. 2010
    ..These studies demonstrate that synphilin-1 can diminish the severity of alpha-synucleinopathy and play a neuroprotective role against A53T alpha-synuclein toxicity in vivo...
  8. ncbi Parkinson's disease genetic mutations increase cell susceptibility to stress: mutant alpha-synuclein enhances H2O2- and Sin-1-induced cell death
    Haibing Jiang
    Department of Psychiatry, Division of Neurobiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Neurobiol Aging 28:1709-17. 2007
    ..These results indicate that genetic mutations in alpha-synuclein may increase neuronal vulnerability to cellular stress in aging and PD pathogenesis...
  9. ncbi Depletion of CBP is directly linked with cellular toxicity caused by mutant huntingtin
    Haibing Jiang
    Division of Neurobiology, Department of Psychiatry, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Neurobiol Dis 23:543-51. 2006
    ..CBP overexpression rescued both acetylated histone levels and cell toxicity. These data suggest that CBP dysfunction and altered gene transcription contribute to mutant htt-induced neurotoxicity...
  10. ncbi Parkinson's disease-associated mutations in leucine-rich repeat kinase 2 augment kinase activity
    Andrew B West
    Institute for Cell Engineering, Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Proc Natl Acad Sci U S A 102:16842-7. 2005
    ..These results suggest a gain-of-function mechanism for LRRK2-linked disease with a central role for kinase activity in the development of PD...
  11. ncbi Inhibitors of LRRK2 kinase attenuate neurodegeneration and Parkinson-like phenotypes in Caenorhabditis elegans and Drosophila Parkinson's disease models
    Zhaohui Liu
    Department of Pharmaceutical Sciences, University of Maryland School of Pharmacy, 20 Penn Street, Baltimore, MD 21201, USA
    Hum Mol Genet 20:3933-42. 2011
    ..These findings indicate that increased kinase activity of LRRK2 is neurotoxic and that inhibition of LRRK2 activity can have a disease-modifying effect. This suggests that inhibition of LRRK2 holds promise as a treatment for PD...
  12. ncbi Endoplasmic reticulum stress and mitochondrial cell death pathways mediate A53T mutant alpha-synuclein-induced toxicity
    Wanli W Smith
    Department of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Hum Mol Genet 14:3801-11. 2005
    ..This study sheds light into the pathogenesis of alpha-synuclein cellular toxicity in PD and provides a cell model for screening PD therapeutic agents...
  13. ncbi Baicalein reduces E46K alpha-synuclein aggregation in vitro and protects cells against E46K alpha-synuclein toxicity in cell models of familiar Parkinsonism
    Mali Jiang
    Division of Neurobiology, Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
    J Neurochem 114:419-29. 2010
    ..Baicalein has potential as a tool to understand the relation between different aggregation species and toxicity, and might be a candidate compound for further validation by using in vivo alpha-syn genetic PD models...
  14. ncbi Gene-environment interactions in Parkinson's disease
    Christopher A Ross
    Department of Psychiatry, Division of Neurobiology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Parkinsonism Relat Disord 13:S309-15. 2007
    ..None of the single models replicate all the features of PD. Genetic models (possibly including more than one mutation) in combination with toxins or other environmental manipulation may provide better models of PD pathogenesis...
  15. ncbi LRRK2 kinase activity mediates toxic interactions between genetic mutation and oxidative stress in a Drosophila model: suppression by curcumin
    Dejun Yang
    Department of Physiology and Pathophysiology, Xi an Jiaotong University School of Medicine, Xi an, Shaanxi, PR China
    Neurobiol Dis 47:385-92. 2012
    ..These studies also identified curcumin as a LRRK2 kinase inhibitor that may be a useful candidate for LRRK2-linked PD intervention...
  16. ncbi A Drosophila model for LRRK2-linked parkinsonism
    Zhaohui Liu
    Department of Psychiatry, Division of Neurobiology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Proc Natl Acad Sci U S A 105:2693-8. 2008
    ..These flies may provide a useful model for studying LRRK2-linked pathogenesis and for future therapeutic screens for PD intervention...
  17. ncbi Alpha-synuclein phosphorylation enhances eosinophilic cytoplasmic inclusion formation in SH-SY5Y cells
    Wanli W Smith
    Department of Psychiatry, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Neurosci 25:5544-52. 2005
    ..These results indicate that phosphorylation of alpha-synuclein at S129 may be important for the formation of inclusions in PD and related alpha synucleinopathies...
  18. ncbi Leptin activates hypothalamic acetyl-CoA carboxylase to inhibit food intake
    Su Gao
    Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Proc Natl Acad Sci U S A 104:17358-63. 2007
    ..Together, these findings highlight site-specific impacts of hypothalamic ACC activation in leptin's anorectic signaling cascade...
  19. ncbi Models for LRRK2-Linked Parkinsonism
    Tianxia Li
    Department of Pharmaceutical Sciences, University of Maryland School of Pharmacy, Baltimore, MD 21201, USA
    Parkinsons Dis 2011:942412. 2011
    ..Here, we review the recent models for LRRK2-linked Parkinsonism and their utility in studying LRRK2 neurobiology, pathogenesis, and potential therapeutics...

Research Grants1

  1. LRRK2 and cellular pathways of Parkinson's Disease
    Wanli Smith; Fiscal Year: 2007
    ....