Shi Pan

Summary

Affiliation: University of Rochester
Country: USA

Publications

  1. ncbi Glutathiolation regulates tumor necrosis factor-alpha-induced caspase-3 cleavage and apoptosis: key role for glutaredoxin in the death pathway
    Shi Pan
    Cardiovascular Research Institute and Department of Medicine, University of Rochester, NY 14642, USA
    Circ Res 100:213-9. 2007
  2. ncbi Molecular mechanisms responsible for the atheroprotective effects of laminar shear stress
    Shi Pan
    Aab Cardiovascular Research Institute, University of Rochester, School of Medicine and Dentistry, Rochester, New York 14642, USA
    Antioxid Redox Signal 11:1669-82. 2009
  3. ncbi Glutaredoxin mediates Akt and eNOS activation by flow in a glutathione reductase-dependent manner
    Jing Wang
    University of Rochester, Cardiovascular Research Institute and Department of Medicine, 601 Elmwood Ave, Rochester, NY 14642, USA
    Arterioscler Thromb Vasc Biol 27:1283-8. 2007
  4. ncbi Glucose 6-phosphate dehydrogenase is regulated through c-Src-mediated tyrosine phosphorylation in endothelial cells
    Shi Pan
    Aab Cardiovascular Research Institute, Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA
    Arterioscler Thromb Vasc Biol 29:895-901. 2009
  5. ncbi Fluid shear stress inhibits vascular inflammation by decreasing thioredoxin-interacting protein in endothelial cells
    Hideyuki Yamawaki
    Center for Cardiovascular Research, University of Rochester, Rochester, New York 14642, USA
    J Clin Invest 115:733-8. 2005
  6. ncbi Flow activates ERK1/2 and endothelial nitric oxide synthase via a pathway involving PECAM1, SHP2, and Tie2
    Lung Kuo Tai
    Cardiovascular Research Institute and Department of Medicine, University of Rochester, New York 14642, USA
    J Biol Chem 280:29620-4. 2005
  7. ncbi Cyclophilin A mediates vascular remodeling by promoting inflammation and vascular smooth muscle cell proliferation
    Kimio Satoh
    Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, 601 Elmwood Ave, Rochester, NY 14642, USA
    Circulation 117:3088-98. 2008
  8. ncbi Etk/Bmx as a tumor necrosis factor receptor type 2-specific kinase: role in endothelial cell migration and angiogenesis
    Shi Pan
    Center for Cardiovascular Research, University of Rochester Medical Center, Rochester, New York 14642, USA
    Mol Cell Biol 22:7512-23. 2002

Collaborators

Detail Information

Publications8

  1. ncbi Glutathiolation regulates tumor necrosis factor-alpha-induced caspase-3 cleavage and apoptosis: key role for glutaredoxin in the death pathway
    Shi Pan
    Cardiovascular Research Institute and Department of Medicine, University of Rochester, NY 14642, USA
    Circ Res 100:213-9. 2007
    ..Furthermore, Grx association with caspase-3 was decreased by tumor necrosis factor-alpha. These findings demonstrate a novel mechanism of caspase-3 regulation by Grx in tumor necrosis factor-alpha-induced apoptosis...
  2. ncbi Molecular mechanisms responsible for the atheroprotective effects of laminar shear stress
    Shi Pan
    Aab Cardiovascular Research Institute, University of Rochester, School of Medicine and Dentistry, Rochester, New York 14642, USA
    Antioxid Redox Signal 11:1669-82. 2009
    ..Thus, high laminar shear stress plays a key role in the prevention of atherosclerosis through its regulation of vascular tone and long-term maintenance of the integrity and function of endothelial cells...
  3. ncbi Glutaredoxin mediates Akt and eNOS activation by flow in a glutathione reductase-dependent manner
    Jing Wang
    University of Rochester, Cardiovascular Research Institute and Department of Medicine, 601 Elmwood Ave, Rochester, NY 14642, USA
    Arterioscler Thromb Vasc Biol 27:1283-8. 2007
    ..Because steady laminar flow exerts an antioxidant effect, we hypothesized that Grx mediates flow induced Akt and eNOS phosphorylation in a GR dependent manner...
  4. ncbi Glucose 6-phosphate dehydrogenase is regulated through c-Src-mediated tyrosine phosphorylation in endothelial cells
    Shi Pan
    Aab Cardiovascular Research Institute, Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA
    Arterioscler Thromb Vasc Biol 29:895-901. 2009
    ..Because tyrosine phosphorylation is a key regulatory pathway for VEGF-mediated endothelial cell (EC) responses, we investigated tyrosine phosphorylation of G6PD and the role of the nonreceptor tyrosine kinase Src...
  5. ncbi Fluid shear stress inhibits vascular inflammation by decreasing thioredoxin-interacting protein in endothelial cells
    Hideyuki Yamawaki
    Center for Cardiovascular Research, University of Rochester, Rochester, New York 14642, USA
    J Clin Invest 115:733-8. 2005
    ..The data suggest that TXNIP and TRX are key components of biomechanical signal transduction and establish them as potentially novel regulators of TNF signaling and inflammation in ECs...
  6. ncbi Flow activates ERK1/2 and endothelial nitric oxide synthase via a pathway involving PECAM1, SHP2, and Tie2
    Lung Kuo Tai
    Cardiovascular Research Institute and Department of Medicine, University of Rochester, New York 14642, USA
    J Biol Chem 280:29620-4. 2005
    ..These results establish Tie2 transactivation via PECAM1 as an early event in flow-mediated mechanotransduction and suggest an important role for a PECAM1-SHP2-Tie2 pathway in flow-mediated signal transduction...
  7. ncbi Cyclophilin A mediates vascular remodeling by promoting inflammation and vascular smooth muscle cell proliferation
    Kimio Satoh
    Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, 601 Elmwood Ave, Rochester, NY 14642, USA
    Circulation 117:3088-98. 2008
    ....
  8. ncbi Etk/Bmx as a tumor necrosis factor receptor type 2-specific kinase: role in endothelial cell migration and angiogenesis
    Shi Pan
    Center for Cardiovascular Research, University of Rochester Medical Center, Rochester, New York 14642, USA
    Mol Cell Biol 22:7512-23. 2002
    ..While most TNF actions have been attributed to TNFR1, our studies demonstrate that Etk is a TNFR2-specific kinase involved in TNF-induced angiogenic events...