Li Gan

Summary

Affiliation: University of California
Country: USA

Publications

  1. ncbi request reprint Identification of cathepsin B as a mediator of neuronal death induced by Abeta-activated microglial cells using a functional genomics approach
    Li Gan
    AGY Therapeutics, Inc, South San Francisco, California 94080, USA
    J Biol Chem 279:5565-72. 2004
  2. ncbi request reprint SIRT1 protects against microglia-dependent amyloid-beta toxicity through inhibiting NF-kappaB signaling
    Jennifer Chen
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94158, USA
    J Biol Chem 280:40364-74. 2005
  3. ncbi request reprint Therapeutic potential of sirtuin-activating compounds in Alzheimer's disease
    Li Gan
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94158, USA
    Drug News Perspect 20:233-9. 2007
  4. doi request reprint Paths of convergence: sirtuins in aging and neurodegeneration
    Li Gan
    Gladstone Institute of Neurological Disease, 1650 Owens Street, San Francisco, CA 94158, USA
    Neuron 58:10-4. 2008
  5. ncbi request reprint Antiamyloidogenic and neuroprotective functions of cathepsin B: implications for Alzheimer's disease
    Sarah Mueller-Steiner
    Gladstone Institute of Neurological Disease, University of California, San Francisco, 1650 Owens Street, 94158, USA
    Neuron 51:703-14. 2006
  6. pmc Cystatin C-cathepsin B axis regulates amyloid beta levels and associated neuronal deficits in an animal model of Alzheimer's disease
    Binggui Sun
    Gladstone Institute of Neurological Disease, University of California San Francisco, San Francisco, CA 94158, USA
    Neuron 60:247-57. 2008
  7. pmc Cathepsin B degrades amyloid-β in mice expressing wild-type human amyloid precursor protein
    Chao Wang
    Gladstone Institute of Neurological Diseases, San Francisco, California 94158, USA
    J Biol Chem 287:39834-41. 2012
  8. pmc Selective targeting of microglia by quantum dots
    S Sakura Minami
    Gladstone Institute of Neurological Disease, 1650 Owens St, San Francisco, CA 94158, USA
    J Neuroinflammation 9:22. 2012
  9. pmc Phospholipase A2 reduction ameliorates cognitive deficits in a mouse model of Alzheimer's disease
    Rene O Sanchez-Mejia
    Gladstone Institute of Neurological Disease, San Francisco, California 94158, USA
    Nat Neurosci 11:1311-8. 2008
  10. pmc Progranulin deficiency promotes neuroinflammation and neuron loss following toxin-induced injury
    Lauren Herl Martens
    Gladstone Institute of Cardiovascular Disease, San Francisco, California 94158, USA
    J Clin Invest 122:3955-9. 2012

Collaborators

Detail Information

Publications24

  1. ncbi request reprint Identification of cathepsin B as a mediator of neuronal death induced by Abeta-activated microglial cells using a functional genomics approach
    Li Gan
    AGY Therapeutics, Inc, South San Francisco, California 94080, USA
    J Biol Chem 279:5565-72. 2004
    ..Our results suggest an essential role for secreted cathepsin B in neuronal death mediated by Abeta-activated inflammatory response...
  2. ncbi request reprint SIRT1 protects against microglia-dependent amyloid-beta toxicity through inhibiting NF-kappaB signaling
    Jennifer Chen
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94158, USA
    J Biol Chem 280:40364-74. 2005
    ..They also implicate SIRT1 in this pathway and highlight the therapeutic potential of resveratrol and other sirtuin-activating compounds in Alzheimer disease...
  3. ncbi request reprint Therapeutic potential of sirtuin-activating compounds in Alzheimer's disease
    Li Gan
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94158, USA
    Drug News Perspect 20:233-9. 2007
    ..In this review, we discuss the potential role of the sirtuin pathway in modifying the pathogenic processes in Alzheimer's disease...
  4. doi request reprint Paths of convergence: sirtuins in aging and neurodegeneration
    Li Gan
    Gladstone Institute of Neurological Disease, 1650 Owens Street, San Francisco, CA 94158, USA
    Neuron 58:10-4. 2008
    ..We will also examine the potential and challenges of targeting sirtuin pathways therapeutically...
  5. ncbi request reprint Antiamyloidogenic and neuroprotective functions of cathepsin B: implications for Alzheimer's disease
    Sarah Mueller-Steiner
    Gladstone Institute of Neurological Disease, University of California, San Francisco, 1650 Owens Street, 94158, USA
    Neuron 51:703-14. 2006
    ..Thus, CatB likely fulfills antiamyloidogenic and neuroprotective functions. Insufficient CatB activity might promote AD; increasing CatB activity could counteract the neuropathology of this disease...
  6. pmc Cystatin C-cathepsin B axis regulates amyloid beta levels and associated neuronal deficits in an animal model of Alzheimer's disease
    Binggui Sun
    Gladstone Institute of Neurological Disease, University of California San Francisco, San Francisco, CA 94158, USA
    Neuron 60:247-57. 2008
    ....
  7. pmc Cathepsin B degrades amyloid-β in mice expressing wild-type human amyloid precursor protein
    Chao Wang
    Gladstone Institute of Neurological Diseases, San Francisco, California 94158, USA
    J Biol Chem 287:39834-41. 2012
    ..These findings support the notion that enhancing CatB activity could lower Aβ, especially Aβ42, in AD patients with or without familial mutations...
  8. pmc Selective targeting of microglia by quantum dots
    S Sakura Minami
    Gladstone Institute of Neurological Disease, 1650 Owens St, San Francisco, CA 94158, USA
    J Neuroinflammation 9:22. 2012
    ..Targeting the delivery of biologically active compounds to microglia could help elucidate these roles and facilitate the therapeutic modulation of microglial functions in neurological diseases...
  9. pmc Phospholipase A2 reduction ameliorates cognitive deficits in a mouse model of Alzheimer's disease
    Rene O Sanchez-Mejia
    Gladstone Institute of Neurological Disease, San Francisco, California 94158, USA
    Nat Neurosci 11:1311-8. 2008
    ..Inhibition of GIVA-PLA(2) may be beneficial in the treatment and prevention of Alzheimer's disease...
  10. pmc Progranulin deficiency promotes neuroinflammation and neuron loss following toxin-induced injury
    Lauren Herl Martens
    Gladstone Institute of Cardiovascular Disease, San Francisco, California 94158, USA
    J Clin Invest 122:3955-9. 2012
    ..These findings suggest that PGRN deficiency may cause increased neuron loss in other forms of CNS injury accompanied by neuroinflammation...
  11. pmc Imbalance between GABAergic and Glutamatergic Transmission Impairs Adult Neurogenesis in an Animal Model of Alzheimer's Disease
    Binggui Sun
    Gladstone Institute of Neurological Disease, University of California, San Francisco, 94158, USA
    Cell Stem Cell 5:624-33. 2009
    ..Abeta-induced increases in GABAergic neurotransmission or an imbalance between GABAergic and glutamatergic neurotransmission may contribute to impaired neurogenesis in AD...
  12. pmc CX3CR1 protein signaling modulates microglial activation and protects against plaque-independent cognitive deficits in a mouse model of Alzheimer disease
    Seo Hyun Cho
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94158, USA
    J Biol Chem 286:32713-22. 2011
    ..Our findings identify CX3CR1 as a key microglial pathway in protecting against AD-related cognitive deficits that are associated with aberrant microglial activation and elevated inflammatory cytokines...
  13. pmc Acetylation of tau inhibits its degradation and contributes to tauopathy
    Sang Won Min
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA
    Neuron 67:953-66. 2010
    ..Inhibiting p300 with a small molecule promoted tau deacetylation and eliminated p-tau associated with tauopathy. Modulating tau acetylation could be a new therapeutic strategy to reduce tau-mediated neurodegeneration...
  14. pmc Poly(ADP-ribose)polymerase-1 modulates microglial responses to amyloid β
    Tiina M Kauppinen
    Department of Neurology, University of California, San Francisco, and Veterans Affairs Medical Center, 4150 Clement Street 127, San Francisco, CA 94121, USA
    J Neuroinflammation 8:152. 2011
    ..The purpose of this study was to evaluate whether PARP-1 activation is involved in Aβ-induced microglial activation, and whether PARP-1 inhibition can modify microglial responses to Aβ...
  15. doi request reprint Manipulation of gene expression in the central nervous system with lentiviral vectors
    Binggui Sun
    Department of Neurology, Gladstone Institute of Neurological Disease, University of California, San Francisco, San Francisco, CA, USA
    Methods Mol Biol 670:155-68. 2011
    ..Here, we describe the preparation and purification of lentiviral vectors and methods of lentiviral infection in primary neural cultures and in brain regions of interest by stereotaxic injection...
  16. ncbi request reprint Intracellularly generated amyloid-beta peptide counteracts the antiapoptotic function of its precursor protein and primes proapoptotic pathways for activation by other insults in neuroblastoma cells
    Luke Esposito
    Gladstone Institute of Neurological Disease, Department of Neurology, University of California, San Francisco, California, USA
    J Neurochem 91:1260-74. 2004
    ..We conclude that Abeta, especially intracellular Abeta, counteracts the antiapoptotic function of its precursor protein and predisposes cells to p53-mediated, and possibly other, proapoptotic pathways...
  17. doi request reprint Poly(ADP-ribose) polymerase-1-induced NAD(+) depletion promotes nuclear factor-κB transcriptional activity by preventing p65 de-acetylation
    Tiina M Kauppinen
    Department of Neurology, University of California, San Francisco, CA 94121, USA
    Biochim Biophys Acta 1833:1985-91. 2013
    ..These findings demonstrate that PARP-1-induced changes in NAD(+) levels can modulate NF-κB transcriptional activity through effects on p65 acetylation...
  18. pmc Argyrophilic grain disease differs from other tauopathies by lacking tau acetylation
    Lea Tenenholz Grinberg
    Memory and Aging Center, Department of Neurology University of California, San Francisco, 675 Nelson Rising Lane, San Francisco, CA 94158, USA
    Acta Neuropathol 125:581-93. 2013
    ..Tau acetylation as a key modification for the propagation tau toxicity deserves further investigation...
  19. ncbi request reprint New non-viral method for gene transfer into primary cells
    Oliver Gresch
    amaxa GmbH, Cologne, Germany
    Methods 33:151-63. 2004
    ....
  20. pmc Neurogenic responses to amyloid-beta plaques in the brain of Alzheimer's disease-like transgenic (pPDGF-APPSw,Ind) mice
    Li Gan
    Department of Anatomy and Cell Biology, University of North Dakota School of Medicine, Grand Forks, ND 58202, USA
    Neurobiol Dis 29:71-80. 2008
    ..The neurogenic responses of NPCs to A beta plaques suggest that experimental approaches to promote de novo neurogenesis may potentially improve neurocognitive function and provide an effective therapy for AD...
  21. ncbi request reprint Temporal response of neural progenitor cells to disease onset and progression in amyotrophic lateral sclerosis-like transgenic mice
    Liying Chi
    Department of Anatomy and Cell Biology, University of North Dakota School of Medicine, Grand Forks, ND 58202, USA
    Stem Cells Dev 16:579-88. 2007
    ....
  22. ncbi request reprint Sulfated polymannuroguluronate, a novel anti-AIDS drug candidate, inhibits T cell apoptosis by combating oxidative damage of mitochondria
    Benchun Miao
    Department of Pharmacology, Marine Drug and Food Institute, Ocean University of China, Qingdao 266003, People s Republic of China
    Mol Pharmacol 68:1716-27. 2005
    ..All these might shed new light on the understanding of anti-AIDS functions of SPMG by protecting T cells of persons infected with human immunodeficiency virus...
  23. ncbi request reprint Regulation of the timing of MNTB neurons by short-term and long-term modulation of potassium channels
    Leonard K Kaczmarek
    Department of Pharmacology, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520, USA
    Hear Res 206:133-45. 2005
    ....
  24. ncbi request reprint Neuregulin-1 suppresses muscarinic receptor expression and acetylcholine-activated muscarinic K+ channels in cardiac myocytes
    Byron D Ford
    Department of Anatomy and Neurobiology, Morehouse School of Medicine, 720 Westview Drive, SW, MRC 223, Atlanta, GA 30310, USA
    Biochem Biophys Res Commun 308:23-8. 2003
    ..These data suggest that neuregulins can regulate cardiac parasympathetic tone and may be involved in the pathogenesis of cardiac arrhythmias and heart failure...

Research Grants2

  1. Cathepsin B and cystatin C in AD-related neuronal damage
    Li Gan; Fiscal Year: 2005
    ..These studies will shed light on the potential role of cysC in AD pathogenesis and further our understanding on the CatB-mediated neuronal damage in AD. ..
  2. The Role of Cathepsin B and Cystatin C in Alzheimer's Disease
    Li Gan; Fiscal Year: 2010
    ..Confirmation that the CatB-CysC axis action acts in a complementary manner with NEP would lay the foundation for designing effective Abeta clearance strategies. ..