05B4 Pan, Shi - Thomas Jefferson University 111C
Thomas Jefferson University
Sidney Kimmel Medical College
Department of Medicine

Pan, Shi

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Shi Pan

Shi Pan, PhD

Contact Dr. Pan

1020 Locust Street
Suite 543G
Philadelphia, PA 19107

(215) 503-4264
(215) 503-5731 fax

Medical School

University of Tokyo - 1998
PhD Molecular and Cellular Biology, University of Tokyo - 1998

University Appointment

Research Assistant Professor

Research & Clinical Interests

Dr. Pan is interested in the redox-sensitive molecular mechanisms in cardiovascular diseases. One of her research interests is the role of redox molecules in the modulation of protein function and cell signaling. Her studies have demonstrated for the first time that caspase-3 is modified by S-glutathiolation, a redox-sensitive posttranslational modification. More importantly, this modification plays a key regulatory role in caspase-3 cleavage and cell death. Her studies on glucose 6-phosphate dehydrogenase, the key enzyme of pentose phosphate pathway producing NADPH, have found that this enzyme is regulated by Src-mediated tyrosine phosphorylation, and this phosphorylation is crucial in VEGF-mediated cellular events. Currently she studies the regulation of mitochondria function in physiological and pathological settings because mitochondria are the key-determinants of cellular redox, energy metabolism and cell fate. Particularly, she is interested in the molecular mechanisms by which cellular redox and signaling regulate mitochondrial ROS generation, calcium uptake and permeability. She hopes these studies will provide insight into the role of mitochondria in cardiac muscle cells and help develop therapeutic strategies for the treatment of heart diseases.

Publications

Most Recent Peer-Reviewed Publications

  1. Downregulation of adenine nucleotide translocator 1 exacerbates tumor necrosis factor-α-mediated cardiac inflammatory responses
  2. ADP protects cardiac mitochondria under severe oxidative stress
  3. Prodeath signaling of G protein-coupled receptor kinase 2 in cardiac myocytes after ischemic stress occurs via extracellular signal-regulated kinase-dependent heat shock protein 90-mediated mitochondrial targeting
  4. Molecular identities of mitochondrial Ca 2+ influx mechanism: Updated passwords for accessing mitochondrial Ca 2+-linked health: And disease
  5. Distinctive characteristics and functions of multiple mitochondrial Ca 2+ influx mechanisms
  6. Molecular mechanisms responsible for the atheroprotective effects of laminar shear stress
  7. Glucose 6-phosphate dehydrogenase is regulated through c-src-mediated tyrosine phosphorylation in endothelial cells
  8. Cyclophilin a mediates vascular remodeling by promoting inflammation and vascular smooth muscle cell proliferation
  9. Glutaredoxin mediates Akt and eNOS activation by flow in a glutathione reductase-dependent manner
  10. Glutathiolation regulates tumor necrosis factor-α-induced caspase-3 cleavage and apoptosis: Key role for glutaredoxin in the death pathway
  11. Flow activates ERK1/2 and endothelial nitric oxide synthase via a pathway involving PEC 05B4 AM1, SHP2, and Tie2
  12. Fluid shear stress inhibits vascular inflammation by decreasing thioredoxin-interacting protein in endothelial cells
  13. Etk/Bmx as a tumor necrosis factor receptor type 2-specific kinase: Role in endothelial cell migration and angiogenesis
  14. Vascular endothelial growth factor isoforms display distinct activities in promoting tumor angiogenesis at different anatomic sites
  15. NFATz: A novel Rel similarity domain containing protein
  16. Molecular cloning and functional characterization of murine cDNA encoding transcription factor NFATc
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