Hai Feng Zhang, PhD
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Extensive Research Description
My main interestis heart and vascular diseases caused by inflammation. Excessive/chronicinflammatory responses (e.g., TNF) and increases in reactive oxygen species(ROS) represent common pathogenic mechanism for atherosclerosis. The vascularcell that primarily limits the inflammatory and atherosclerotic process is thevascular endothelial cells (EC). Inflammation/ROS induces EC dysfunction bydisturbing normal homeostasis, relaxation and survival. These defects in ECfunction are mediated by cytokine/redox-regulated signal transduction and genetranscription. My experiments are designed to dissect signal pathways duringinflammatory responses. We have identified that AIP1 plays important roles inTNF signaling pathways in EC by interacting with ASK1,TRAF2 and RIP1. AIP1'sother functions such as tumor suppression are under investigation.
Coauthors
Selected Publications
- AIP1 functions as an endogenous inhibitor of VEGFR2-mediated signaling and inflammatory angiogenesis in mice.Zhang H, He Y, Dai S, Xu Z, Luo Y, Wan T, Luo D, Jones D, Tang S, Chen H, Sessa WC, Min W. AIP1 functions as an endogenous inhibitor of VEGFR2-mediated signaling and inflammatory angiogenesis in mice. The Journal Of Clinical Investigation 2008, 118:3904-16.
- AIP1 recruits phosphatase PP2A to ASK1 in tumor necrosis factor-induced ASK1-JNK activation.Min W, Lin Y, Tang S, Yu L, Zhang H, Wan T, Luhn T, Fu H, Chen H. AIP1 recruits phosphatase PP2A to ASK1 in tumor necrosis factor-induced ASK1-JNK activation. Circulation Research 2008, 102:840-8.
- AIP1 is critical in transducing IRE1-mediated endoplasmic reticulum stress response.Luo D, He Y, Zhang H, Yu L, Chen H, Xu Z, Tang S, Urano F, Min W. AIP1 is critical in transducing IRE1-mediated endoplasmic reticulum stress response. The Journal Of Biological Chemistry 2008, 283:11905-12.
- SENP1 mediates TNF-induced desumoylation and cytoplasmic translocation of HIPK1 to enhance ASK1-dependent apoptosis.Li X, Luo Y, Yu L, Lin Y, Luo D, Zhang H, He Y, Kim YO, Kim Y, Tang S, Min W. SENP1 mediates TNF-induced desumoylation and cytoplasmic translocation of HIPK1 to enhance ASK1-dependent apoptosis. Cell Death And Differentiation 2008, 15:739-50.
- RIP1-mediated AIP1 phosphorylation at a 14-3-3-binding site is critical for tumor necrosis factor-induced ASK1-JNK/p38 activation.Zhang H, Zhang H, Lin Y, Li J, Pober JS, Min W. RIP1-mediated AIP1 phosphorylation at a 14-3-3-binding site is critical for tumor necrosis factor-induced ASK1-JNK/p38 activation. The Journal Of Biological Chemistry 2007, 282:14788-96.
- Endothelial-specific expression of mitochondrial thioredoxin improves endothelial cell function and reduces atherosclerotic lesions.Zhang H, Luo Y, Zhang W, He Y, Dai S, Zhang R, Huang Y, Bernatchez P, Giordano FJ, Shadel G, Sessa WC, Min W. Endothelial-specific expression of mitochondrial thioredoxin improves endothelial cell function and reduces atherosclerotic lesions. The American Journal Of Pathology 2007, 170:1108-20.
- AIP1/DAB2IP, a novel member of the Ras-GAP family, transduces TRAF2-induced ASK1-JNK activation.Zhang H, Zhang R, Luo Y, D'Alessio A, Pober JS, Min W. AIP1/DAB2IP, a novel member of the Ras-GAP family, transduces TRAF2-induced ASK1-JNK activation. The Journal Of Biological Chemistry 2004, 279:44955-65.
- Inhibition of the expression of the human RNase P protein subunits Rpp21, Rpp25, Rpp29 by external guide sequences (EGSs) and siRNA.Zhang H, Altman S. Inhibition of the expression of the human RNase P protein subunits Rpp21, Rpp25, Rpp29 by external guide sequences (EGSs) and siRNA. Journal Of Molecular Biology 2004, 342:1077-83.