Vincent T Marchesi

Summary

Affiliation: Yale University
Country: USA

Publications

  1. doi request reprint Alzheimer's dementia begins as a disease of small blood vessels, damaged by oxidative-induced inflammation and dysregulated amyloid metabolism: implications for early detection and therapy
    Vincent T Marchesi
    Department of Pathology, Boyer Center for Molecular Medicine, Yale University, 295 Congress Ave, P O Box 9812, New Haven, CT 06536 0812, USA
    FASEB J 25:5-13. 2011
  2. doi request reprint Alzheimer's disease and CADASIL are heritable, adult-onset dementias that both involve damaged small blood vessels
    Vincent T Marchesi
    Department of Pathology, Yale University, New Haven, CT, 06536 0812, USA
    Cell Mol Life Sci 71:949-55. 2014
  3. doi request reprint Alzheimer's disease 2012: the great amyloid gamble
    Vincent T Marchesi
    Department of Pathology and the Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, Connecticut 06536, USA
    Am J Pathol 180:1762-7. 2012
  4. pmc An alternative interpretation of the amyloid Abeta hypothesis with regard to the pathogenesis of Alzheimer's disease
    Vincent T Marchesi
    Department of Pathology, Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, CT 06510, USA
    Proc Natl Acad Sci U S A 102:9093-8. 2005
  5. ncbi request reprint The relevance of research on red cell membranes to the understanding of complex human disease: a personal perspective
    Vincent T Marchesi
    Department of Pathology, Boyer Center for Molecular Medicine, Yale University, New Haven, CT 06511, USA
    Annu Rev Pathol 3:1-9. 2008
  6. pmc The AHNAKs are a class of giant propeller-like proteins that associate with calcium channel proteins of cardiomyocytes and other cells
    Akihiko Komuro
    Departments of Pathology and Immunobiology, Boyer Center for Molecular Medicine, Yale University School of Medicine, 295 Congress Avenue, New Haven, CT 06510, USA
    Proc Natl Acad Sci U S A 101:4053-8. 2004
  7. pmc A scaffold protein, AHNAK1, is required for calcium signaling during T cell activation
    Didi Matza
    Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06510, USA
    Immunity 28:64-74. 2008
  8. pmc Requirement for AHNAK1-mediated calcium signaling during T lymphocyte cytolysis
    Didi Matza
    Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06510, USA
    Proc Natl Acad Sci U S A 106:9785-90. 2009

Collaborators

  • Didi Matza
  • Richard A Flavell
  • Akihiko Komuro
  • Abdallah Badou
  • Koichi S Kobayashi
  • Yutaka Masuda
  • Mithilesh K Jha
  • Andrey Antov
  • Tim Willinger
  • Shomyseh Sanjabi
  • Diane McMahon-Pratt
  • Karen Goldsmith-Pestana
  • Roger Babbitt
  • Koichi Kobayashi
  • Murat Gunel

Detail Information

Publications8

  1. doi request reprint Alzheimer's dementia begins as a disease of small blood vessels, damaged by oxidative-induced inflammation and dysregulated amyloid metabolism: implications for early detection and therapy
    Vincent T Marchesi
    Department of Pathology, Boyer Center for Molecular Medicine, Yale University, 295 Congress Ave, P O Box 9812, New Haven, CT 06536 0812, USA
    FASEB J 25:5-13. 2011
    ..The novel addition offered here is the speculation that low-abundance, gain-of-function somatic mutations of the amyloid precursor protein may be part of the triggering mechanism...
  2. doi request reprint Alzheimer's disease and CADASIL are heritable, adult-onset dementias that both involve damaged small blood vessels
    Vincent T Marchesi
    Department of Pathology, Yale University, New Haven, CT, 06536 0812, USA
    Cell Mol Life Sci 71:949-55. 2014
    ....
  3. doi request reprint Alzheimer's disease 2012: the great amyloid gamble
    Vincent T Marchesi
    Department of Pathology and the Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, Connecticut 06536, USA
    Am J Pathol 180:1762-7. 2012
    ..This review explores the wisdom of that approach...
  4. pmc An alternative interpretation of the amyloid Abeta hypothesis with regard to the pathogenesis of Alzheimer's disease
    Vincent T Marchesi
    Department of Pathology, Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, CT 06510, USA
    Proc Natl Acad Sci U S A 102:9093-8. 2005
    ....
  5. ncbi request reprint The relevance of research on red cell membranes to the understanding of complex human disease: a personal perspective
    Vincent T Marchesi
    Department of Pathology, Boyer Center for Molecular Medicine, Yale University, New Haven, CT 06511, USA
    Annu Rev Pathol 3:1-9. 2008
    ..I describe here how studies of red blood cell membrane proteins evolved and how results from those studies still inform present-day research...
  6. pmc The AHNAKs are a class of giant propeller-like proteins that associate with calcium channel proteins of cardiomyocytes and other cells
    Akihiko Komuro
    Departments of Pathology and Immunobiology, Boyer Center for Molecular Medicine, Yale University School of Medicine, 295 Congress Avenue, New Haven, CT 06510, USA
    Proc Natl Acad Sci U S A 101:4053-8. 2004
    ..AHNAK2 is predicted to have a PDZ domain within its N-terminal, nonrepeating domain, which may mediate these interactions...
  7. pmc A scaffold protein, AHNAK1, is required for calcium signaling during T cell activation
    Didi Matza
    Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06510, USA
    Immunity 28:64-74. 2008
    ..Thus, AHNAK1 plays an essential role in T cell Ca2+ signaling through Cav1 channels, triggered via TCR activation; therefore, AHNAK1 is a potential target for therapeutic intervention...
  8. pmc Requirement for AHNAK1-mediated calcium signaling during T lymphocyte cytolysis
    Didi Matza
    Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06510, USA
    Proc Natl Acad Sci U S A 106:9785-90. 2009
    ..Our results demonstrate an AHNAK1-dependent mechanism controlling calcium entry during CTL effector function...