SUZANNE Y GUENETTE

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. pmc FE65 as a link between VLDLR and APP to regulate their trafficking and processing
    Sonya B Dumanis
    Department of Neuroscience, Georgetown University Medical Center, 3970 Reservoir Road NW, Washington, DC 20057 1464, USA
    Mol Neurodegener 7:9. 2012
  2. pmc Essential roles for the FE65 amyloid precursor protein-interacting proteins in brain development
    Suzanne Guenette
    Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Charlestown, MA 02129 4404, USA
    EMBO J 25:420-31. 2006
  3. ncbi request reprint Mechanisms of Abeta clearance and catabolism
    SUZANNE Y GUENETTE
    Mass General Institute for Neurodegenerative Disease, Massachusetts General Hospital East, 114 16th St, Charlestown, MA 02129 4404, USA
    Neuromolecular Med 4:147-60. 2003
  4. ncbi request reprint Progress toward valid transgenic mouse models for Alzheimer's disease
    S Y Guenette
    Department of Neurology, Massachusetts General Hospital, Charlestown 02129, USA
    Neurobiol Aging 20:201-11. 1999
  5. ncbi request reprint Astrocytes: a cellular player in Abeta clearance and degradation
    SUZANNE Y GUENETTE
    Center for Aging Genetics and Neurodegeneration, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129 4404, USA
    Trends Mol Med 9:279-80. 2003
  6. ncbi request reprint Low-density lipoprotein receptor-related protein levels and endocytic function are reduced by overexpression of the FE65 adaptor protein, FE65L1
    SUZANNE Y GUENETTE
    Genetics and Aging Research Unit, Center for Aging Genetics and Neurodegeneration, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neurochem 82:755-62. 2002
  7. ncbi request reprint A role for APP in motility and transcription?
    SUZANNE Y GUENETTE
    Genetics and Aging Research Unit, Massachusetts General Hospital, Harvard Medical School, 114 16th Street, Charlestown, MA 02129 4404, USA
    Trends Pharmacol Sci 23:203-5; discussion 205-6. 2002
  8. ncbi request reprint Evidence against association of the FE65 gene (APBB1) intron 13 polymorphism in Alzheimer's patients
    S Y Guenette
    Genetics and Aging Unit, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA
    Neurosci Lett 296:17-20. 2000
  9. ncbi request reprint Generation of the beta-amyloid peptide and the amyloid precursor protein C-terminal fragment gamma are potentiated by FE65L1
    Yang Chang
    Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129 4404, USA
    J Biol Chem 278:51100-7. 2003
  10. pmc FE65 proteins regulate NMDA receptor activation-induced amyloid precursor protein processing
    Jaehong Suh
    Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts, USA
    J Neurochem 119:377-88. 2011

Research Grants

  1. Biological Role of the FE65 Protein/APP Interactions
    Suzanne Guenette; Fiscal Year: 2007
  2. ROLE OF HFE65 PROTEINS IN ALZHEIMER'S DISEASE.
    Suzanne Guenette; Fiscal Year: 2003
  3. Biological Role of the FE65 Protein/APP Interactions
    Suzanne Guenette; Fiscal Year: 2009

Collaborators

Detail Information

Publications11

  1. pmc FE65 as a link between VLDLR and APP to regulate their trafficking and processing
    Sonya B Dumanis
    Department of Neuroscience, Georgetown University Medical Center, 3970 Reservoir Road NW, Washington, DC 20057 1464, USA
    Mol Neurodegener 7:9. 2012
    ..In the present study, we tested whether FE65 can interact with another ApoE receptor, VLDLR, thereby altering its trafficking and processing, and whether FE65 can serve as a linker between APP and VLDLR...
  2. pmc Essential roles for the FE65 amyloid precursor protein-interacting proteins in brain development
    Suzanne Guenette
    Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Charlestown, MA 02129 4404, USA
    EMBO J 25:420-31. 2006
    ..The defects observed in the double knockout may also involve the family of Ena/Vasp proteins, which participate in actin cytoskeleton remodeling and interact with the WW domains of FE65 proteins...
  3. ncbi request reprint Mechanisms of Abeta clearance and catabolism
    SUZANNE Y GUENETTE
    Mass General Institute for Neurodegenerative Disease, Massachusetts General Hospital East, 114 16th St, Charlestown, MA 02129 4404, USA
    Neuromolecular Med 4:147-60. 2003
    ..This review will examine the data obtained from studies performed in knockout and transgenic mice on the proteases; the cells and the physiological mechanisms that play a part in the removal of Abeta from the brain...
  4. ncbi request reprint Progress toward valid transgenic mouse models for Alzheimer's disease
    S Y Guenette
    Department of Neurology, Massachusetts General Hospital, Charlestown 02129, USA
    Neurobiol Aging 20:201-11. 1999
    ..Crosses of APP transgenic mice with mice modified for known AD risk factors and "humanizing" the mouse may be necessary for complete replication of AD...
  5. ncbi request reprint Astrocytes: a cellular player in Abeta clearance and degradation
    SUZANNE Y GUENETTE
    Center for Aging Genetics and Neurodegeneration, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129 4404, USA
    Trends Mol Med 9:279-80. 2003
  6. ncbi request reprint Low-density lipoprotein receptor-related protein levels and endocytic function are reduced by overexpression of the FE65 adaptor protein, FE65L1
    SUZANNE Y GUENETTE
    Genetics and Aging Research Unit, Center for Aging Genetics and Neurodegeneration, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neurochem 82:755-62. 2002
    ..These data show that FE65L1 can differentially affect the metabolic fate of APP and LRP. In addition, these data suggest that the LRP decrease observed in FE65L1 overexpressing cells may in part contribute to altered APP processing...
  7. ncbi request reprint A role for APP in motility and transcription?
    SUZANNE Y GUENETTE
    Genetics and Aging Research Unit, Massachusetts General Hospital, Harvard Medical School, 114 16th Street, Charlestown, MA 02129 4404, USA
    Trends Pharmacol Sci 23:203-5; discussion 205-6. 2002
    ..Future studies are required to understand the full implications of these new findings and to determine whether therapeutic strategies for Alzheimer's disease should take these putative functions into account...
  8. ncbi request reprint Evidence against association of the FE65 gene (APBB1) intron 13 polymorphism in Alzheimer's patients
    S Y Guenette
    Genetics and Aging Unit, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA
    Neurosci Lett 296:17-20. 2000
    ..We conclude that the association of the FE65 intron 13 polymorphism with AD, if any, is smaller than previously reported...
  9. ncbi request reprint Generation of the beta-amyloid peptide and the amyloid precursor protein C-terminal fragment gamma are potentiated by FE65L1
    Yang Chang
    Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129 4404, USA
    J Biol Chem 278:51100-7. 2003
    ..Finally, although FE65L1 increases APP C-terminal domain production, it does not mediate the APP-dependent transcriptional activation observed with FE65...
  10. pmc FE65 proteins regulate NMDA receptor activation-induced amyloid precursor protein processing
    Jaehong Suh
    Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts, USA
    J Neurochem 119:377-88. 2011
    ..Our results indicate that the FE65 proteins contribute to physiological APP processing and accumulation of APP metabolic products resulting from NMDAR activation...
  11. ncbi request reprint HtrA2 regulates beta-amyloid precursor protein (APP) metabolism through endoplasmic reticulum-associated degradation
    Henri J Huttunen
    Neurobiology of Disease Laboratory, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA
    J Biol Chem 282:28285-95. 2007
    ..Based on these results we suggest a novel function for HtrA2 as a regulator of APP metabolism through ER-associated degradation...

Research Grants10

  1. Biological Role of the FE65 Protein/APP Interactions
    Suzanne Guenette; Fiscal Year: 2007
    ..In addition, we will gain insight into the role of the FE65 proteins in cellular signaling events that are critical for brain function. ..
  2. ROLE OF HFE65 PROTEINS IN ALZHEIMER'S DISEASE.
    Suzanne Guenette; Fiscal Year: 2003
    ..of hFE65L to LRP contribute to the extracellular pool of APPs and Abeta? Does the FE65L-APP interaction have an effect on intracellular Abeta42 production? Does FE65L act as an adaptor protein form a tripartite complex with APP and LRP? ..
  3. Biological Role of the FE65 Protein/APP Interactions
    Suzanne Guenette; Fiscal Year: 2009
    ..In addition, we will gain insight into the role of the FE65 proteins in cellular signaling events that are critical for brain function. ..