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Department of Basic Medical Science

 

Mingui Fu

Mingui Fu, Ph.D.

Assistant Professor
Department of Basic Medical Sciences
MG101A
Office: 816-235-5881
Fax: 816-235-6444

fum@umkc.edu

 

 

 

Education:

Peking University Health Science Center, China
Ph.D. (2000)

UT Southwestern Medical Center, Dallas
Postdoctoral Fellow (2006)

 

Research Interest

Our research interest is to identify the molecular regulators controlling inflammatory response and immunity and study their contribution to human inflammatory diseases such as septic shock, atherosclerosis and inflammatory-associated malignancy. Currently, we are working on a novel CCCH-zinc finger containing protein family in the regulation of macrophage inflammation and immunity. Our recent results suggest that this protein family negatively regulates JNK and NF-κB signaling by multiple mechanisms. Now we have generated the knockout mouse model and stable cell lines overexpressing or knocking down these genes. By using these animal and cellular models, we will dissect the function and molecular mechanisms of this protein family in inflammation and inflammatory diseases.

 

Recent Publications

Liang J, Wang J, Asim A, Kolattukudy PE, Fu M. A novel CCCH-zinc finger protein family regulates proinflammatory activation of macrophages. J Biol Chem, 2008, 283:6337-6346.

Liang J, Song W, Tromp G, Kolattukudy PE, and Fu M. Genome-wide survey and expression profiling of CCCH-zinc finger family reveals a functional module in macrophage activation. PLoS ONE. 2008, 3(8):e2880.

Liang J, Lei T, Song Y, Yanes N, Qi Y, Fu M. RNA-destabilizing factor tristetraprolin negatively regulates NF-κB signaling. J Biol Chem, 2009, 284:29383-90.

Qi Y, Liang J, She Z-G, Cai Y, Wang J, Lei T, Stallcup WB, Fu M. MCP-induced protein 1 suppresses TNFα-induced VCAM-1 expression in human endothelial cells. FEBS Lett, 2010,584:3065-72.

Liang J, Saad Y, Lei T, Wang J, Qi D, Yang Q, Kolattukudy PE, Fu M. MCP-induced protein 1 acts as a deubiquitinase to negatively regulate JNK and NF-κB signaling by targeting TRAF family. J Exp Med, 2010 (in press).