George R Jackson

Summary

Affiliation: University of California
Country: USA

Publications

  1. ncbi request reprint Human wild-type tau interacts with wingless pathway components and produces neurofibrillary pathology in Drosophila
    George R Jackson
    Neurogenetics Program, Department of Neurology, University of California Los Angeles, School of Medicine, 710 Westwood Plaza, 90095, USA
    Neuron 34:509-19. 2002
  2. pmc A Drosophila model of ALS: human ALS-associated mutation in VAP33A suggests a dominant negative mechanism
    Anuradha Ratnaparkhi
    Department of Neurology, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, California, United States of America
    PLoS ONE 3:e2334. 2008
  3. pmc Guide to understanding Drosophila models of neurodegenerative diseases
    George R Jackson
    Department of Neurology and Center for Neurobehavioral Genetics, Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine at the University of California, Los Angeles, United States of America
    PLoS Biol 6:e53. 2008
  4. pmc Dissociation of tau toxicity and phosphorylation: role of GSK-3beta, MARK and Cdk5 in a Drosophila model
    Shreyasi Chatterjee
    Department of Neurology, Neurogenetics and Movement Disorders Programs, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA
    Hum Mol Genet 18:164-77. 2009
  5. ncbi request reprint A genomic screen for modifiers of tauopathy identifies puromycin-sensitive aminopeptidase as an inhibitor of tau-induced neurodegeneration
    Stanislav L Karsten
    Program in Neurogenetics, Department of Neurology, Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA
    Neuron 51:549-60. 2006
  6. ncbi request reprint A Drosophila model of mutant human parkin-induced toxicity demonstrates selective loss of dopaminergic neurons and dependence on cellular dopamine
    Tzu Kang Sang
    Neurogenetics Program, Department of Neurology, National Tsing Hua University, Taiwan, Republic of China
    J Neurosci 27:981-92. 2007
  7. pmc Functional genomic screen and network analysis reveal novel modifiers of tauopathy dissociated from tau phosphorylation
    Surendra S Ambegaokar
    Department of Neurology, University of Texas Medical Branch, 301 University Blvd, MRB 10 138, Galveston, TX 77555, USA
    Hum Mol Genet 20:4947-77. 2011
  8. pmc Bacterial artificial chromosome transgenic mice expressing a truncated mutant parkin exhibit age-dependent hypokinetic motor deficits, dopaminergic neuron degeneration, and accumulation of proteinase K-resistant alpha-synuclein
    Xiao hong Lu
    Center for Neurobehavioral Genetics, Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California 90095, USA
    J Neurosci 29:1962-76. 2009
  9. pmc Disruption of glycerol metabolism by RNAi targeting of genes encoding glycerol kinase results in a range of phenotype severity in Drosophila
    Patrick J Wightman
    Department of Human Genetics, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, California, United States of America
    PLoS ONE 8:e71664. 2013
  10. pmc Interaction between eye pigment genes and tau-induced neurodegeneration in Drosophila melanogaster
    Surendra S Ambegaokar
    Neuroscience Interdepartmental Ph D Program, Brain Research Institute, Center for Neurobehavioral Genetics, Semel Institute for Neuroscience and Human Behavior, and Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA
    Genetics 186:435-42. 2010

Research Grants

Collaborators

Detail Information

Publications20

  1. ncbi request reprint Human wild-type tau interacts with wingless pathway components and produces neurofibrillary pathology in Drosophila
    George R Jackson
    Neurogenetics Program, Department of Neurology, University of California Los Angeles, School of Medicine, 710 Westwood Plaza, 90095, USA
    Neuron 34:509-19. 2002
    ..The genetic system we have established provides a powerful reagent for identification of novel modifiers of tau-induced neurodegeneration that may serve as future therapeutic targets...
  2. pmc A Drosophila model of ALS: human ALS-associated mutation in VAP33A suggests a dominant negative mechanism
    Anuradha Ratnaparkhi
    Department of Neurology, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, California, United States of America
    PLoS ONE 3:e2334. 2008
    ..This new fly model of ALS, with its robust pathological phenotypes, should for the first time allow the power of unbiased screens in Drosophila to be applied to study of motor neuron diseases...
  3. pmc Guide to understanding Drosophila models of neurodegenerative diseases
    George R Jackson
    Department of Neurology and Center for Neurobehavioral Genetics, Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine at the University of California, Los Angeles, United States of America
    PLoS Biol 6:e53. 2008
  4. pmc Dissociation of tau toxicity and phosphorylation: role of GSK-3beta, MARK and Cdk5 in a Drosophila model
    Shreyasi Chatterjee
    Department of Neurology, Neurogenetics and Movement Disorders Programs, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA
    Hum Mol Genet 18:164-77. 2009
    ..These data have important implications for the understanding and interpretation of animal models of tauopathy...
  5. ncbi request reprint A genomic screen for modifiers of tauopathy identifies puromycin-sensitive aminopeptidase as an inhibitor of tau-induced neurodegeneration
    Stanislav L Karsten
    Program in Neurogenetics, Department of Neurology, Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA
    Neuron 51:549-60. 2006
    ..Further investigation is warranted in defining the role of PSA and other genes identified here as potential therapeutic targets in tauopathy...
  6. ncbi request reprint A Drosophila model of mutant human parkin-induced toxicity demonstrates selective loss of dopaminergic neurons and dependence on cellular dopamine
    Tzu Kang Sang
    Neurogenetics Program, Department of Neurology, National Tsing Hua University, Taiwan, Republic of China
    J Neurosci 27:981-92. 2007
    ..These results support a model in which the vulnerability of DA neurons to parkin-induced neurotoxicity results from the interaction of mutant parkin with cytoplasmic dopamine...
  7. pmc Functional genomic screen and network analysis reveal novel modifiers of tauopathy dissociated from tau phosphorylation
    Surendra S Ambegaokar
    Department of Neurology, University of Texas Medical Branch, 301 University Blvd, MRB 10 138, Galveston, TX 77555, USA
    Hum Mol Genet 20:4947-77. 2011
    ..These findings suggest therapeutic targets other than mitigation of tau phosphorylation...
  8. pmc Bacterial artificial chromosome transgenic mice expressing a truncated mutant parkin exhibit age-dependent hypokinetic motor deficits, dopaminergic neuron degeneration, and accumulation of proteinase K-resistant alpha-synuclein
    Xiao hong Lu
    Center for Neurobehavioral Genetics, Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California 90095, USA
    J Neurosci 29:1962-76. 2009
    ..Our study underscores the need to further explore the putative link between parkin dominant toxicity and PD...
  9. pmc Disruption of glycerol metabolism by RNAi targeting of genes encoding glycerol kinase results in a range of phenotype severity in Drosophila
    Patrick J Wightman
    Department of Human Genetics, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, California, United States of America
    PLoS ONE 8:e71664. 2013
    ....
  10. pmc Interaction between eye pigment genes and tau-induced neurodegeneration in Drosophila melanogaster
    Surendra S Ambegaokar
    Neuroscience Interdepartmental Ph D Program, Brain Research Institute, Center for Neurobehavioral Genetics, Semel Institute for Neuroscience and Human Behavior, and Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA
    Genetics 186:435-42. 2010
    ..Interaction with nucleotide-derived pigments or increased lysosomal dysregulation are potential mechanisms. Finally, tau toxicity correlates with increased GSK-3β activity, but not with tau phosphorylation at Ser202/Thr205...
  11. ncbi request reprint Hydrolethalus syndrome is caused by a missense mutation in a novel gene HYLS1
    Lisa Mee
    Department of Human Genetics, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, CA, USA
    Hum Mol Genet 14:1475-88. 2005
    ..The Drosophila melanogaster model confirmed these findings and provides evidence for the significance of the mutation both in vitro and in vivo...
  12. pmc Association of GSK3B with Alzheimer disease and frontotemporal dementia
    Barbara A J Schaffer
    Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, 2506 Gonda, 695 Charles E Young Dr S, Los Angeles, CA 90095 1761, USA
    Arch Neurol 65:1368-74. 2008
    ..As a known tau kinase, GSK3B is a promising candidate gene in the remaining cases of FTD and in AD, for which tau mutations have not been found...
  13. pmc Drosophila models of neurodegenerative disease
    Tzu Kang Sang
    Neurogenetics Program, Department of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA
    NeuroRx 2:438-46. 2005
    ..Here, we provide a general overview of fly models pertinent to trinucleotide repeat expansion disorders, Alzheimer's, and Parkinson's diseases, and highlight key genetic modifiers that have been identified to date using such models...
  14. pmc The downward spiral of tau and autolysosomes: a new hypothesis in neurodegeneration
    Suren S Ambegaokar
    Department of Neurology, University of Texas Medical Branch, Galveston, TX, USA
    Autophagy 8:1144-5. 2012
    ..Recently, studies of the effects of autophagy as a clearance mechanism have uncovered compelling evidence that inducing autophagy can alleviate many pathogenic and behavioral symptoms in animal and cellular models of neurodegeneration...
  15. pmc Glycerol hypersensitivity in a Drosophila model for glycerol kinase deficiency is affected by mutations in eye pigmentation genes
    Patrick J Wightman
    Department of Human Genetics, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, California, United States of America
    PLoS ONE 7:e31779. 2012
    ....
  16. ncbi request reprint Inactivation of Drosophila Apaf-1 related killer suppresses formation of polyglutamine aggregates and blocks polyglutamine pathogenesis
    Tzu Kang Sang
    Neurogenetics Program, Department of Neurology, Neuropsychiatric Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA
    Hum Mol Genet 14:357-72. 2005
    ..These findings suggest that limiting Apaf-1 activity may alleviate both pathological protein aggregation and neuronal cell death in HD...
  17. doi request reprint Demise of the flies: why Drosophila models still matter
    Mathieu F Bakhoum
    Mitchell Center for Neurodegenerative Diseases, Department of Neurology, The University of Texas Medical Branch, Galveston, TX, USA
    Prog Mol Biol Transl Sci 100:483-98. 2011
    ..Here, we will provide a brief overview of some Drosophila models of neurodegenerative disorders with a special focus on our own work...
  18. pmc Normal-repeat-length polyglutamine peptides accelerate aggregation nucleation and cytotoxicity of expanded polyglutamine proteins
    Natalia Slepko
    Department of Psychiatry and Human Behavior, University of California, Irvine, CA 92697 4260, USA
    Proc Natl Acad Sci U S A 103:14367-72. 2006
    ..The results suggest that the overall state of the polyGln protein network in a cellular environment may have a profound effect on the toxic consequences of polyGln expansion and thus may serve as a genetic modifier of age of onset in HD...
  19. ncbi request reprint gamma-cleavage-independent functions of presenilin, nicastrin, and Aph-1 regulate cell-junction organization and prevent tau toxicity in vivo
    Laura E Doglio
    Cavalieri Ottolenghi Scientific Institute, Universita degli Studi di Torino, 10043, Orbassano, Torino, Italy
    Neuron 50:359-75. 2006
    ..These results establish new in vivo molecular functions for the three components of the gamma-secretase complex and reveal a different mechanism that might contribute to neuronal degeneration in Alzheimer's disease...
  20. ncbi request reprint Degradation of tau protein by puromycin-sensitive aminopeptidase in vitro
    Soma Sengupta
    Department of Cell and Molecular Biology, Feinberg School of Medicine at Northwestern University
    Biochemistry 45:15111-9. 2006
    ..These results are consistent with observations that PSA modulates tau levels in vivo and suggest that this enzyme may be involved in tau degradation in human brain...

Research Grants1

  1. Molecular Genetics of Polyglutamine-Induced Degeneration
    George Jackson; Fiscal Year: 2003
    ..abstract not available ..