J L Hall

Summary

Affiliation: University of Minnesota
Country: USA

Publications

  1. ncbi Overexpression of Ref-1 inhibits hypoxia and tumor necrosis factor-induced endothelial cell apoptosis through nuclear factor-kappab-independent and -dependent pathways
    J L Hall
    Division of Cardiovascular Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, Mass, USA
    Circ Res 88:1247-53. 2001
  2. ncbi Determinants of vascular smooth muscle cell apoptosis after balloon angioplasty injury. Influence of redox state and cell phenotype
    M J Pollman
    Molecular Vascular Cell Biology Research Laboratory, Brigham and Women s Hospital, Harvard Medical School, Boston, MA, USA
    Circ Res 84:113-21. 1999
  3. ncbi Upregulation of glucose metabolism during intimal lesion formation is coupled to the inhibition of vascular smooth muscle cell apoptosis. Role of GSK3beta
    J L Hall
    Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA
    Diabetes 50:1171-9. 2001

Collaborators

Detail Information

Publications3

  1. ncbi Overexpression of Ref-1 inhibits hypoxia and tumor necrosis factor-induced endothelial cell apoptosis through nuclear factor-kappab-independent and -dependent pathways
    J L Hall
    Division of Cardiovascular Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, Mass, USA
    Circ Res 88:1247-53. 2001
    ..Moreover, it seems that Ref-1 may act as a critical cofactor, mediating the TNF-induced NF-kappaB response in the vascular endothelium...
  2. ncbi Determinants of vascular smooth muscle cell apoptosis after balloon angioplasty injury. Influence of redox state and cell phenotype
    M J Pollman
    Molecular Vascular Cell Biology Research Laboratory, Brigham and Women s Hospital, Harvard Medical School, Boston, MA, USA
    Circ Res 84:113-21. 1999
    ..Angioplasty-induced vascular cell apoptosis may be an important determinant of vascular remodeling and restenosis...
  3. ncbi Upregulation of glucose metabolism during intimal lesion formation is coupled to the inhibition of vascular smooth muscle cell apoptosis. Role of GSK3beta
    J L Hall
    Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA
    Diabetes 50:1171-9. 2001
    ..Taken together, upregulation of glucose metabolism during intimal lesion formation promotes an antiapoptotic signaling pathway that is linked to the inactivation of GSK3beta...