Angela Ho

Summary

Affiliation: Boston University
Country: USA

Publications

  1. pmc Deletion of Mint proteins decreases amyloid production in transgenic mouse models of Alzheimer's disease
    Angela Ho
    Department of Neuroscience, The University of Texas Southwestern Medical Center, Dallas, Texas 75390 9111, USA
    J Neurosci 28:14392-400. 2008
  2. ncbi request reprint Genetic analysis of Mint/X11 proteins: essential presynaptic functions of a neuronal adaptor protein family
    Angela Ho
    Center for Basic Neuroscience, University of Texas Southwestern Medical Center, Dallas, Texas 75390 9111, USA
    J Neurosci 26:13089-101. 2006
  3. pmc Deletion of CASK in mice is lethal and impairs synaptic function
    Deniz Atasoy
    Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX 75390 9111, USA
    Proc Natl Acad Sci U S A 104:2525-30. 2007
  4. pmc A role for Mints in transmitter release: Mint 1 knockout mice exhibit impaired GABAergic synaptic transmission
    Angela Ho
    Center for Basic Neuroscience, Department of Molecular Genetics, and Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX 75390 9111, USA
    Proc Natl Acad Sci U S A 100:1409-14. 2003
  5. pmc Binding of F-spondin to amyloid-beta precursor protein: a candidate amyloid-beta precursor protein ligand that modulates amyloid-beta precursor protein cleavage
    Angela Ho
    The Center for Basic Neuroscience, Department of Molecular Genetics, and Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, NA4 118, Dallas, TX 75390 9111, USA
    Proc Natl Acad Sci U S A 101:2548-53. 2004

Collaborators

Detail Information

Publications5

  1. pmc Deletion of Mint proteins decreases amyloid production in transgenic mouse models of Alzheimer's disease
    Angela Ho
    Department of Neuroscience, The University of Texas Southwestern Medical Center, Dallas, Texas 75390 9111, USA
    J Neurosci 28:14392-400. 2008
    ..These results suggest that the three Mint/X11 proteins regulate Abeta production by a novel mechanism that may have implications for therapeutic approaches to altering APP cleavage in Alzheimer's disease...
  2. ncbi request reprint Genetic analysis of Mint/X11 proteins: essential presynaptic functions of a neuronal adaptor protein family
    Angela Ho
    Center for Basic Neuroscience, University of Texas Southwestern Medical Center, Dallas, Texas 75390 9111, USA
    J Neurosci 26:13089-101. 2006
    ..Our studies thus indicate that Mints are important regulators of presynaptic neurotransmitter release that are essential for mouse survival...
  3. pmc Deletion of CASK in mice is lethal and impairs synaptic function
    Deniz Atasoy
    Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX 75390 9111, USA
    Proc Natl Acad Sci U S A 104:2525-30. 2007
    ....
  4. pmc A role for Mints in transmitter release: Mint 1 knockout mice exhibit impaired GABAergic synaptic transmission
    Angela Ho
    Center for Basic Neuroscience, Department of Molecular Genetics, and Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX 75390 9111, USA
    Proc Natl Acad Sci U S A 100:1409-14. 2003
    ..Our data indicate that Mints 1 and 2 perform redundant synaptic functions that become apparent in Mint 1-deficient mice in inhibitory interneurons because these neurons selectively express higher levels of Mint 1 than Mint 2...
  5. pmc Binding of F-spondin to amyloid-beta precursor protein: a candidate amyloid-beta precursor protein ligand that modulates amyloid-beta precursor protein cleavage
    Angela Ho
    The Center for Basic Neuroscience, Department of Molecular Genetics, and Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, NA4 118, Dallas, TX 75390 9111, USA
    Proc Natl Acad Sci U S A 101:2548-53. 2004
    ..Our data indicate that F-spondin may be an endogenous regulator of APP cleavage, and suggest that the extracellular domains of APP are potential drug targets for interfering with beta-secretase cleavage...