Yadong Huang

Summary

Affiliation: University of California
Country: USA

Publications

  1. pmc Hilar GABAergic interneuron activity controls spatial learning and memory retrieval
    Yaisa Andrews-Zwilling
    Gladstone Institute of Neurological Disease, San Francisco, California, United States of America
    PLoS ONE 7:e40555. 2012
  2. pmc Cellular source-specific effects of apolipoprotein (apo) E4 on dendrite arborization and dendritic spine development
    Sachi Jain
    Gladstone Institute of Neurological Disease, San Francisco, California, United States of America
    PLoS ONE 8:e59478. 2013
  3. pmc Apolipoprotein E4 causes age- and sex-dependent impairments of hilar GABAergic interneurons and learning and memory deficits in mice
    Laura Leung
    Gladstone Institute of Neurological Disease, San Francisco, California, United States of America
    PLoS ONE 7:e53569. 2012
  4. pmc Arf4 determines dentate gyrus-mediated pattern separation by regulating dendritic spine development
    Sachi Jain
    Gladstone Institute of Neurological Disease, San Francisco, California, USA
    PLoS ONE 7:e46340. 2012
  5. ncbi request reprint Apolipoprotein E and Alzheimer disease
    Yadong Huang
    Gladstone Institute of Neurological Disease, Department of Pathology, University of California, San Francisco, CA, USA
    Neurology 66:S79-85. 2006
  6. ncbi request reprint Apolipoprotein E: diversity of cellular origins, structural and biophysical properties, and effects in Alzheimer's disease
    Yadong Huang
    Gladstone Institute of Neurological Disease, Gladstone Institute of Cardiovascular Disease, and the Department of Pathology, University of California, San Francisco, CA 94141 9100, USA
    J Mol Neurosci 23:189-204. 2004
  7. doi request reprint Roles of apolipoprotein E4 (ApoE4) in the pathogenesis of Alzheimer's disease: lessons from ApoE mouse models
    Yadong Huang
    Gladstone Institute of Neurological Disease, Department of Pathology, University of California, San Francisco, CA 94158, USA
    Biochem Soc Trans 39:924-32. 2011
  8. ncbi request reprint Molecular and cellular mechanisms of apolipoprotein E4 neurotoxicity and potential therapeutic strategies
    Yadong Huang
    Gladstone Institute of Neurological Disease, University of California, San Francisco, 1650 Owens Street, San Francisco, CA 94158, USA
    Curr Opin Drug Discov Devel 9:627-41. 2006
  9. ncbi request reprint Abeta-independent roles of apolipoprotein E4 in the pathogenesis of Alzheimer's disease
    Yadong Huang
    the Gladstone Institute of Neurological Disease, University of California, San Francisco, CA 94158, USA
    Trends Mol Med 16:287-94. 2010
  10. doi request reprint Mechanisms linking apolipoprotein E isoforms with cardiovascular and neurological diseases
    Yadong Huang
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94158, USA
    Curr Opin Lipidol 21:337-45. 2010

Research Grants

Collaborators

Detail Information

Publications63

  1. pmc Hilar GABAergic interneuron activity controls spatial learning and memory retrieval
    Yaisa Andrews-Zwilling
    Gladstone Institute of Neurological Disease, San Francisco, California, United States of America
    PLoS ONE 7:e40555. 2012
    ....
  2. pmc Cellular source-specific effects of apolipoprotein (apo) E4 on dendrite arborization and dendritic spine development
    Sachi Jain
    Gladstone Institute of Neurological Disease, San Francisco, California, United States of America
    PLoS ONE 8:e59478. 2013
    ..These results indicate that the effects of apoE4 on dendrite arborization, spine density, and spine morphology depend critically on its cellular source, with neuronal apoE4 having more detrimental effects than astrocytic apoE4...
  3. pmc Apolipoprotein E4 causes age- and sex-dependent impairments of hilar GABAergic interneurons and learning and memory deficits in mice
    Laura Leung
    Gladstone Institute of Neurological Disease, San Francisco, California, United States of America
    PLoS ONE 7:e53569. 2012
    ..These findings suggest that the sex-dependent effects of apoE4 on developing AD is in part attributable to inherent sex-based differences in the numbers of hilar GABAergic interneurons, which is further modulated by apoE genotype...
  4. pmc Arf4 determines dentate gyrus-mediated pattern separation by regulating dendritic spine development
    Sachi Jain
    Gladstone Institute of Neurological Disease, San Francisco, California, USA
    PLoS ONE 7:e46340. 2012
    ..Our findings suggest that Arf4 is a critical modulator of DG-mediated pattern separation by regulating dendritic spine development...
  5. ncbi request reprint Apolipoprotein E and Alzheimer disease
    Yadong Huang
    Gladstone Institute of Neurological Disease, Department of Pathology, University of California, San Francisco, CA, USA
    Neurology 66:S79-85. 2006
    ..Thus, multiple molecular and cellular mechanisms should be considered when anti-AD drugs are developed based on apoE studies...
  6. ncbi request reprint Apolipoprotein E: diversity of cellular origins, structural and biophysical properties, and effects in Alzheimer's disease
    Yadong Huang
    Gladstone Institute of Neurological Disease, Gladstone Institute of Cardiovascular Disease, and the Department of Pathology, University of California, San Francisco, CA 94141 9100, USA
    J Mol Neurosci 23:189-204. 2004
    ..Some of these mechanisms might be suitable targets for the development of new treatments for AD...
  7. doi request reprint Roles of apolipoprotein E4 (ApoE4) in the pathogenesis of Alzheimer's disease: lessons from ApoE mouse models
    Yadong Huang
    Gladstone Institute of Neurological Disease, Department of Pathology, University of California, San Francisco, CA 94158, USA
    Biochem Soc Trans 39:924-32. 2011
    ..They also provide useful tools for discovery and development of drugs targeting apoE4's detrimental effects...
  8. ncbi request reprint Molecular and cellular mechanisms of apolipoprotein E4 neurotoxicity and potential therapeutic strategies
    Yadong Huang
    Gladstone Institute of Neurological Disease, University of California, San Francisco, 1650 Owens Street, San Francisco, CA 94158, USA
    Curr Opin Drug Discov Devel 9:627-41. 2006
    ..Thus, multiple molecular and cellular mechanisms should be considered in developing anti-AD drugs that target apoE4...
  9. ncbi request reprint Abeta-independent roles of apolipoprotein E4 in the pathogenesis of Alzheimer's disease
    Yadong Huang
    the Gladstone Institute of Neurological Disease, University of California, San Francisco, CA 94158, USA
    Trends Mol Med 16:287-94. 2010
    ....
  10. doi request reprint Mechanisms linking apolipoprotein E isoforms with cardiovascular and neurological diseases
    Yadong Huang
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94158, USA
    Curr Opin Lipidol 21:337-45. 2010
    ..The purpose of this review is to provide insights into recent advances in mechanisms linking apolipoprotein (apo) E isoforms to cardiovascular and neurological diseases...
  11. pmc Apolipoprotein E fragments present in Alzheimer's disease brains induce neurofibrillary tangle-like intracellular inclusions in neurons
    Y Huang
    Gladstone Institute of Neurological Disease, P O Box 419100, San Francisco, CA 94141 9100, USA
    Proc Natl Acad Sci U S A 98:8838-43. 2001
    ....
  12. pmc Apolipoprotein E4 causes age- and Tau-dependent impairment of GABAergic interneurons, leading to learning and memory deficits in mice
    Yaisa Andrews-Zwilling
    Gladstone Institute of Neurological Disease, University of California, San Francisco, San Francisco, California 94158, USA
    J Neurosci 30:13707-17. 2010
    ..Consequently, reducing Tau and enhancing GABA signaling are potential strategies to treat or prevent apoE4-related Alzheimer's disease...
  13. ncbi request reprint Neuron-specific apolipoprotein e4 proteolysis is associated with increased tau phosphorylation in brains of transgenic mice
    Walter J Brecht
    Gladstone Institute of Neurological Disease, San Francisco, California 94141 9100, USA
    J Neurosci 24:2527-34. 2004
    ..Neuron-specific proteolytic cleavage of apoE4 is associated with increased phosphorylation of tau and may play a key role in the development of AD-related neuronal deficits...
  14. ncbi request reprint Increased tau phosphorylation in apolipoprotein E4 transgenic mice is associated with activation of extracellular signal-regulated kinase: modulation by zinc
    Faith M Harris
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94141 9100, USA
    J Biol Chem 279:44795-801. 2004
    ..Thus, increased tau phosphorylation in apoE4 transgenic mice was associated with Erk activation and could be modified by zinc, suggesting that apoE4 and zinc act in concert to contribute to the pathogenesis of AD...
  15. pmc GABAergic interneuron dysfunction impairs hippocampal neurogenesis in adult apolipoprotein E4 knockin mice
    Gang Li
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA
    Cell Stem Cell 5:634-45. 2009
    ..These findings suggest that GABAergic signaling can be targeted to mitigate the deleterious effects of apoE4 on neurogenesis...
  16. ncbi request reprint Astroglial regulation of apolipoprotein E expression in neuronal cells. Implications for Alzheimer's disease
    Faith M Harris
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94141 9100, USA
    J Biol Chem 279:3862-8. 2004
    ..Thus, neuronal expression of apoE is regulated by a diffusible factor or factors released from astrocytes, and this regulation depends on the activity of the Erk kinase pathway in neurons...
  17. ncbi request reprint Reactivity of apolipoprotein E4 and amyloid beta peptide: lysosomal stability and neurodegeneration
    Zhong Sheng Ji
    Gladstone Institute of Neurological Disease, Gladstone Institute of Cardiovascular Disease, University of California, San Francisco, California 94158, USA
    J Biol Chem 281:2683-92. 2006
    ..Thus, apoE4 and Abeta1-42 may work in concert in neurons to increase lysosome formation while increasing the susceptibility of lysosomal membranes to disruption, release of lysosomal enzymes into the cytosol, and neuronal degeneration...
  18. pmc Apolipoprotein (apo) E4 enhances amyloid beta peptide production in cultured neuronal cells: apoE structure as a potential therapeutic target
    Shiming Ye
    Gladstone Institute of Neurological Disease, 1650 Owens Street, San Francisco, CA 94158, USA
    Proc Natl Acad Sci U S A 102:18700-5. 2005
    ..These findings provide insights into why apoE4 is associated with increased risk for Alzheimer's disease and may represent a potential target for drug development...
  19. doi request reprint Intron-3 retention/splicing controls neuronal expression of apolipoprotein E in the CNS
    Qin Xu
    Gladstone Institute of Neurological Disease, San Francisco, California 94158, USA
    J Neurosci 28:1452-9. 2008
    ..Thus, neuronal expression of apoE is controlled by transcription of apoE-I3 under normal conditions and by processing of apoE-I3 into mature apoE mRNA in response to injury...
  20. pmc Cellular source of apolipoprotein E4 determines neuronal susceptibility to excitotoxic injury in transgenic mice
    Manuel Buttini
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158 2261, USA
    Am J Pathol 177:563-9. 2010
    ..Thus, an imbalance between astrocytic (excitoprotective) and neuronal (neurotoxic) apoE4 expression may increase susceptibility to diverse neurological diseases involving excitotoxic mechanisms...
  21. ncbi request reprint Modulation of Alzheimer-like synaptic and cholinergic deficits in transgenic mice by human apolipoprotein E depends on isoform, aging, and overexpression of amyloid beta peptides but not on plaque formation
    Manuel Buttini
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94141 9100, USA
    J Neurosci 22:10539-48. 2002
    ..Thus, apoE3, but not apoE4, delays age- and Abeta-dependent synaptic deficits through a plaque-independent mechanism. This difference could contribute to the differential effects of apoE isoforms on the risk and onset of AD...
  22. ncbi request reprint Profile and regulation of apolipoprotein E (ApoE) expression in the CNS in mice with targeting of green fluorescent protein gene to the ApoE locus
    Qin Xu
    Gladstone Institute of Neurological Disease, San Francisco, California 94158, USA
    J Neurosci 26:4985-94. 2006
    ..EGFPapoE reporter mice will be useful for studying the regulation of apoE expression in the CNS and might provide insights into the diverse mechanisms of apoE4-related neurodegeneration...
  23. pmc Lipid- and receptor-binding regions of apolipoprotein E4 fragments act in concert to cause mitochondrial dysfunction and neurotoxicity
    Shengjun Chang
    Gladstone Institute of Neurological Disease, 1650 Owens Street, San Francisco, CA 94158, USA
    Proc Natl Acad Sci U S A 102:18694-9. 2005
    ..Thus, the lipid- and receptor-binding regions in apoE4 fragments act together to cause mitochondrial dysfunction and neurotoxicity, which may be important in Alzheimer's disease pathogenesis...
  24. pmc Reducing human apolipoprotein E levels attenuates age-dependent Aβ accumulation in mutant human amyloid precursor protein transgenic mice
    Nga Bien-Ly
    Gladstone Institute of Neurological Disease, San Francisco, California 94158, USA
    J Neurosci 32:4803-11. 2012
    ..Moreover, Cre-mediated APOE4 gene excision in hippocampal astrocytes significantly reduced insoluble Aβ in adult mice. Thus, reducing, rather than increasing, apoE expression is an attractive approach to lowering brain Aβ levels...
  25. pmc Small molecule structure correctors abolish detrimental effects of apolipoprotein E4 in cultured neurons
    Hung Kai Chen
    Gladstone Center for Translational Research, San Francisco, California 94158, USA
    J Biol Chem 287:5253-66. 2012
    ..Our results serve as a proof of concept that pharmacological intervention with apoE4 structure correctors negates apoE4 detrimental effects in neuronal cells and could be further developed as an Alzheimer disease therapeutic...
  26. pmc Rosiglitazone increases dendritic spine density and rescues spine loss caused by apolipoprotein E4 in primary cortical neurons
    Jens Brodbeck
    Gladstone Institute of Neurological Disease and Gladstone Institute of Cardiovascular Disease, The J David Gladstone Institutes, 1650 Owens Street, San Francisco, CA 94158, USA
    Proc Natl Acad Sci U S A 105:1343-6. 2008
    ..Rosiglitazone rescued this detrimental effect. Thus, rosiglitazone might improve cognition in AD patients by increasing dendritic spine density...
  27. ncbi request reprint Apolipoprotein E4 potentiates amyloid beta peptide-induced lysosomal leakage and apoptosis in neuronal cells
    Zhong Sheng Ji
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94141 9100, USA
    J Biol Chem 277:21821-8. 2002
    ....
  28. pmc Greater medial temporal hypometabolism and lower cortical amyloid burden in ApoE4-positive AD patients
    Manja Lehmann
    Department of Neurology, Memory and Aging Center, University of California, San Francisco, California, USA
    J Neurol Neurosurg Psychiatry 85:266-73. 2014
    ..We aimed to assess the relationship between amyloid deposition, glucose metabolism and ApoE4 genotype in a clinically heterogeneous population of AD patients...
  29. pmc Apolipoprotein E4 domain interaction mediates detrimental effects on mitochondria and is a potential therapeutic target for Alzheimer disease
    Hung Kai Chen
    Gladstone Center for Translational Research, San Francisco, California 94158, USA
    J Biol Chem 286:5215-21. 2011
    ..These results suggest that pharmacological intervention with small molecules that disrupt apoE4 domain interaction is a potential therapeutic approach for apoE4-carrying AD subjects...
  30. pmc C-terminal-truncated apolipoprotein (apo) E4 inefficiently clears amyloid-beta (Abeta) and acts in concert with Abeta to elicit neuronal and behavioral deficits in mice
    Nga Bien-Ly
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA
    Proc Natl Acad Sci U S A 108:4236-41. 2011
    ..Thus, the C-terminal-truncated apoE4 fragment inefficiently clears Aβ peptides and acts in concert with low levels of Aβ to elicit neuronal and behavioral deficits in mice...
  31. pmc Apolipoprotein E4: a causative factor and therapeutic target in neuropathology, including Alzheimer's disease
    Robert W Mahley
    Gladstone Institute of Neurological Disease, 1650 Owens Street, San Francisco, CA 94158, USA
    Proc Natl Acad Sci U S A 103:5644-51. 2006
    ....
  32. pmc Structure-dependent impairment of intracellular apolipoprotein E4 trafficking and its detrimental effects are rescued by small-molecule structure correctors
    Jens Brodbeck
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94158, USA
    J Biol Chem 286:17217-26. 2011
    ..Correcting the pathological structure of apoE4 by disrupting domain interaction is a potential therapeutic approach to treat or prevent AD related to apoE4...
  33. ncbi request reprint Apolipoprotein A-V: a potential modulator of plasma triglyceride levels in Turks
    Ugur Hodoglugil
    Gladstone Institute of Cardiovascular Disease, University of California, San Francisco, San Francisco, CA, USA
    J Lipid Res 47:144-53. 2006
    ..At least one of these alleles was present in approximately 40% of the Turks. Similar associations were observed for -1131T>C and S19W in white Americans living in San Francisco, California...
  34. ncbi request reprint Evidence for differential effects of apoE3 and apoE4 on HDL metabolism
    Paul C R Hopkins
    Gladstone Institute of Cardiovascular Disease, University of California, San Francisco, CA 94141 9100, USA
    J Lipid Res 43:1881-9. 2002
    ....
  35. ncbi request reprint Apolipoprotein E4 domain interaction occurs in living neuronal cells as determined by fluorescence resonance energy transfer
    Qin Xu
    Gladstone Institute of Neurological Disease, University of California, San Francisco, CA 94141, USA
    J Biol Chem 279:25511-6. 2004
    ..Thus, apoE4 domain interaction occurs in living neuronal cells and may be a molecular basis for apoE4-related neurodegeneration...
  36. doi request reprint Small-molecule structure correctors target abnormal protein structure and function: structure corrector rescue of apolipoprotein E4-associated neuropathology
    Robert W Mahley
    Gladstone Institute of Neurological Disease, 1650 Owens Street, San Francisco, California 94158, United States
    J Med Chem 55:8997-9008. 2012
    ..Structure-corrector-based therapies could prove to be highly effective for the treatment of many protein-misfolding diseases...
  37. doi request reprint Apolipoprotein e sets the stage: response to injury triggers neuropathology
    Robert W Mahley
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA
    Neuron 76:871-85. 2012
    ..Here, we review data supporting the hypothesis that apoE4 (> apoE3 > apoE2) has direct neurotoxic effects and highlight studies showing that blocking domain interaction reverses these detrimental effects...
  38. pmc Direct reprogramming of mouse and human fibroblasts into multipotent neural stem cells with a single factor
    Karen L Ring
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA
    Cell Stem Cell 11:100-9. 2012
    ..Thus, self-renewable and multipotent iNSCs without tumorigenic potential can be generated directly from fibroblasts by reprogramming...
  39. pmc Apolipoprotein (apo) E4 enhances HIV-1 cell entry in vitro, and the APOE epsilon4/epsilon4 genotype accelerates HIV disease progression
    Trevor D Burt
    Division of Experimental Medicine, Department of Medicine, and Division of Neonatology, Department of Pediatrics, University of California, San Francisco, CA 94110, USA
    Proc Natl Acad Sci U S A 105:8718-23. 2008
    ....
  40. pmc Putting cholesterol in its place: apoE and reverse cholesterol transport
    Robert W Mahley
    Gladstone Institute of Neurological Disease and Gladstone Institute of Cardiovascular Disease, San Francisco, California 94158, USA
    J Clin Invest 116:1226-9. 2006
    ..In lower species, these large HDLs are not atherogenic. Thus, CETP might not be essential for reverse cholesterol transport in humans, raising hope of using a CETP inhibitor to elevate HDL levels...
  41. pmc Carboxyl-terminal-truncated apolipoprotein E4 causes Alzheimer's disease-like neurodegeneration and behavioral deficits in transgenic mice
    Faith M Harris
    Gladstone Institute of Neurological Disease, San Francisco, CA 94141 9100, USA
    Proc Natl Acad Sci U S A 100:10966-71. 2003
    ..Inhibiting their formation might inhibit apoE4-associated neuronal deficits...
  42. ncbi request reprint Effect of domain interaction on apolipoprotein E levels in mouse brain
    Gayathri Ramaswamy
    Gladstone Institute of Neurological Disease, Departments of Pathology and Neurology, and Cardiovascular Research Institute, University of California, San Francisco, California 94158
    J Neurosci 25:10658-63. 2005
    ..Cells may recognize apoE4 and Arg-61 apoE as misfolded proteins and target them for degradation or accumulation. Thus, degradation/accumulation or lower levels of apoE4 may contribute to the association of apoE4 with Alzheimer's disease...
  43. pmc Apolipoprotein E: structure determines function, from atherosclerosis to Alzheimer's disease to AIDS
    Robert W Mahley
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA
    J Lipid Res 50:S183-8. 2009
    ..The next phase in our understanding of apoE will be characterized by clinical intervention to prevent or reverse the detrimental effects of apoE4 by modulating its structure or blocking the pathological processes it mediates...
  44. ncbi request reprint AAV serotype-1 mediates early onset of gene expression in mouse hearts and results in better therapeutic effect
    H Su
    Cardiovascular Research Institute, University of California San Francisco, 513 Parnassus Avenue, San Francisco, CA 94143, USA
    Gene Ther 13:1495-502. 2006
    ..Thus, AAV1 mediates earlier and higher transgene expression in myocardium and better therapeutic effects...
  45. ncbi request reprint AAV serotype 1 mediates more efficient gene transfer to pig myocardium than AAV serotype 2 and plasmid
    H Su
    Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA 94143 0793, USA
    J Gene Med 10:33-41. 2008
    ..AAV-mediated VEGF gene transfer can also induce neovascular formation in the pig myocardium...
  46. ncbi request reprint Apolipoprotein E: from atherosclerosis to Alzheimer's disease and beyond
    R W Mahley
    Gladstone Institute of Cardiovascular Disease, San Francisco, CA 94141 9100, USA
    Curr Opin Lipidol 10:207-17. 1999
    ..The isoform-specific effects of apolipoprotein E are currently being unraveled through detailed structure and function studies of this protein...
  47. ncbi request reprint Apolipoprotein (apo) E4 and Alzheimer's disease: unique conformational and biophysical properties of apoE4 can modulate neuropathology
    R W Mahley
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA
    Acta Neurol Scand Suppl 185:8-14. 2006
    ..It is predictable that apoE4 acts through various pathways to cause cognitive decline and neurodegeneration...
  48. pmc ApoE and TDP-43 neuropathology in two siblings with familial FTLD-motor neuron disease
    Keith A Vossel
    Department of Neurology, University of California, San Francisco, CA, USA
    Neurocase 19:295-301. 2013
    ..Although differences seen in a sibling pair could arise due to chance, these findings raise the possibility that apoE4 exacerbates brain pathology in FTLD through formation of neurotoxic apoE fragments and interactions with TDP-43...
  49. pmc Kynurenine 3-monooxygenase inhibition in blood ameliorates neurodegeneration
    Daniel Zwilling
    Gladstone Institute of Neurological Disease, University of California, San Francisco, San Francisco, CA 94158, USA
    Cell 145:863-74. 2011
    ..These findings support a critical link between tryptophan metabolism in the blood and neurodegeneration, and they provide a foundation for treatment of neurodegenerative diseases...
  50. ncbi request reprint Detrimental effects of apolipoprotein E4: potential therapeutic targets in Alzheimer's disease
    Robert W Mahley
    Gladstone Institute of Neurological Disease 1650 Owens Street, San Francisco, CA 94158, USA
    Curr Alzheimer Res 4:537-40. 2007
    ..Structural features that distinguish apoE4 and apoE3 determine their functional differences and hold the key to understanding how apoE4 is involved in Alzheimer's disease...
  51. ncbi request reprint Common polymorphisms of ATP binding cassette transporter A1, including a functional promoter polymorphism, associated with plasma high density lipoprotein cholesterol levels in Turks
    Ugur Hodoglugil
    Gladstone Institute of Cardiovascular Disease, 1650 Owens Street, San Francisco, CA 94158, USA
    Atherosclerosis 183:199-212. 2005
    ..In conclusion, we describe a functional promoter polymorphism (C-14T) and a coding sequence variant (V771M) of ABCA1 and their interactions with two other variants (R219K and I883M) on plasma HDL-C levels in Turks...
  52. pmc Atherogenic remnant lipoproteins: role for proteoglycans in trapping, transferring, and internalizing
    Robert W Mahley
    Gladstone Institute of Neurological Disease and Gladstone Institute of Cardiovascular Disease, San Francisco, California 94158, USA
    J Clin Invest 117:94-8. 2007
    ....
  53. ncbi request reprint Age-related hippocampal changes in Bcl-2:Bax ratio, oxidative stress, redox-active iron and apoptosis associated with aluminum-induced neurodegeneration: increased susceptibility with aging
    J Savory
    Department of Pathology, University of Virginia Health Sciences Center, Charlottesville 22908, USA
    Neurotoxicology 20:805-17. 1999
    ..These are novel observations which may have important implications for aiding in our understanding of the pathogenesis of neurodegeneration occurring in Alzheimer's disease...
  54. pmc Alzheimer mechanisms and therapeutic strategies
    Yadong Huang
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA
    Cell 148:1204-22. 2012
    ..However, investigative and drug development efforts should be diversified to fully address the multifactoriality of the disease...
  55. ncbi request reprint Electrostatic interactions of S4 voltage sensor in Shaker K+ channel
    D M Papazian
    Department of Physiology, School of Medicine, University of California, Los Angeles 90024, USA
    Neuron 14:1293-301. 1995
    ..A simple structural hypothesis is proposed to account for the effects of the rescued double mutant combinations on the relative stabilities of open and closed channel conformations...
  56. ncbi request reprint Apolipoprotein E2 transgenic rabbits. Modulation of the type III hyperlipoproteinemic phenotype by estrogen and occurrence of spontaneous atherosclerosis
    Y Huang
    Gladstone Institute of Cardiovascular Disease, Cardiovascular Research Institute, University of California, San Francisco, California 94141-9100, USA
    J Biol Chem 272:22685-94. 1997
    ..Therefore, high plasma levels of human apoE2 in transgenic rabbits result in a type III HLP phenotype, in which males have both more severe hyperlipidemia and more extensive atherosclerosis than females...
  57. pmc Gene expression in papillary thyroid carcinoma reveals highly consistent profiles
    Y Huang
    Human Cancer Genetics Program, Comprehensive Cancer Center, Department of Pathology, Divisions of Sensory Biophysics and Endocrinology and Nuclear Medicine, Ohio State University, Columbus, OH 43210, USA
    Proc Natl Acad Sci U S A 98:15044-9. 2001
    ..We conclude that, despite its clinical heterogeneity, PTC is characterized by consistent and specific molecular changes. These findings reveal clues to the molecular pathways involved in PTC and may provide biomarkers for clinical use...
  58. ncbi request reprint Overexpression and accumulation of apolipoprotein E as a cause of hypertriglyceridemia
    Y Huang
    Gladstone Institute of Cardiovascular Disease, and Pathology, University of California, San Francisco, California 94141 9100, USA
    J Biol Chem 273:26388-93. 1998
    ..The apoE3-overexpressing mice will be useful for studying the pathophysiology of this disorder...
  59. ncbi request reprint Apolipoprotein E2 reduces the low density lipoprotein level in transgenic mice by impairing lipoprotein lipase-mediated lipolysis of triglyceride-rich lipoproteins
    Y Huang
    Gladstone Institute of Cardiovascular Disease, University of California, San Francisco, California 94141 9100, USA
    J Biol Chem 273:17483-90. 1998
    ..The increase in plasma cholesterol caused by apoE2 is due mostly to impaired clearance, whereas the increase in plasma triglycerides is caused mainly by apoE2-impaired lipolysis of triglyceride-rich lipoproteins...
  60. ncbi request reprint Genetic factors precipitating type III hyperlipoproteinemia in hypolipidemic transgenic mice expressing human apolipoprotein E2
    Y Huang
    Gladstone Institute of Cardiovascular Disease, University of California, San Francisco, USA
    Arterioscler Thromb Vasc Biol 17:2817-24. 1997
    ....
  61. ncbi request reprint Hypolipidemic and hyperlipidemic phenotypes in transgenic mice expressing human apolipoprotein E2
    Y Huang
    Gladstone Institute of Cardiovascular Disease, University of California, San Francisco, California 94141 9100, USA
    J Biol Chem 271:29146-51. 1996
    ..This animal model provides the opportunity to study the factors that cause hypolipidemia and those that precipitate the hyperlipidemia of type III HLP...
  62. ncbi request reprint ApoE genotype accounts for the vast majority of AD risk and AD pathology
    Jacob Raber
    Departments of Behavioral Neuroscience and Neurology, L470, ONPRC, Oregon Health and Science University, 3181 S W Sam Jackson Park Road, Portland, OR 97201, USA
    Neurobiol Aging 25:641-50. 2004
    ..Thus, the epidemiologic and basic science evidence suggest that apoE genotype accounts for the vast majority of AD risk and pathology...

Research Grants5

  1. APOE EXPRESSION LEVEL MODULATES VLDL METABOLISM
    Yadong Huang; Fiscal Year: 2000
    ..abstract_text> ..
  2. APOE EXPRESSION LEVEL MODULATES VLDL METABOLISM
    Yadong Huang; Fiscal Year: 2001
    ..abstract_text> ..
  3. APOE EXPRESSION LEVEL MODULATES VLDL METABOLISM
    Yadong Huang; Fiscal Year: 2002
    ..abstract_text> ..
  4. APOE EXPRESSION LEVEL MODULATES VLDL METABOLISM
    Yadong Huang; Fiscal Year: 2003
    ..abstract_text> ..