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Qiutang Li, Ph.D.

by sysadmin last modified Mar 09, 2009 01:13 PM

Research interest

Cornea is the transparent part of eye and free of blood vessels or any cloudy or opaque areas. The corneal epithelium, located on the most-front region, is important for absorbing oxygen and cell nutrients from tears and protection of cornea damages from environmental stimuli. Failure to repair the injuries and abrasions would cause scarring and impair vision. Our group has been studying the homeostasis of stratified squamous epithelium in both skin and cornea. We are especially interested in the role of IKK1 and 14-3-3sigma in the epithelial development, homeostasis, wound healing, and tumorigenesis. We currently investigate the molecular and genetic roles of IKK1 and 14-3-3-sigma in the corneal epithelium development and wound healing process, using gene knockout mice as models. We anticipate to gain a better understanding of some corneal diseases and to provide new molecular basis for prevention and treatment of such diseases.

Current Position

Assistant Professor, Department of Ophthalmology & Visual Sciences
Assistant Professor, James Graham Brown Cancer Center, Stem Cell Institute since 2006

Research Specialties

NF-kappaB signaling pathway, epidermal development, corneal epithelium, knockout and transgenic mice, lentiviral vectors

Contact Information

q.li@louisville.edu

University of Louisville

Department of Ophthalmology and Visual Sciences

301 East Muhammad Ali Boulevard

Louisville, KY40202

502-852-2409 Fax: 502-852-6909

Current Grants

The project described is supported by a COBRA funding from NIH Grant Number P20RR018733 from the National Center for Research Resources and a startup founding from James Graham Brown Cancer Center of the University of Louisville.

Select Publications

Li Q, Lu Q, Estepa G and Verma IM. Identification of 14-3-3 sigma mutation causing cutaneous abnormality in Repeated Epilation mutant mouse. PNAS 102(44):15977-82. (2005)

Li Q, Lu Q, Bottero V, Estepa G, Morrison L, Mercurio F and Verma IM. Enhanced NF-B activation and cellular function in macrophages lacking IB kinase 1 (IKK1). PNAS 102(35):12425-30. (2005)

Li Q, Withoff S, and Verma IM. Inflammation-associated cancer: NF-kB is the lynchpin. Trends Immunol. 26(6):318-25.(2005)

Li Q, Verma IM. NF-kappaB regulation in the immune system. Nat Rev Immunol. 2(10):725-34(2002).

Li Q, Estepa G., Memet S., Israel A., and Verma IM. Complete lack of NF-B activity in IKK1 and IKK2 double deficient mice: Additional defect in neurulation. Genes Dev. 14(14):1729-33 (2000).

Li Q, Lu Q, Hwang JY, Buscher D, Lee KF, Izpisua-Belmonte JC, and Verma IM. IKK1-deficient mice exhibit abnormal development of skin and skeleton. Genes Dev 13(10), 1322-8 (1999).

Li, Q., Van Antwerp, D., Mercurio, F., Lee, K.F., and Verma, I.M. Severe liver degeneration in mice lacking the IkappaB kinase 2 gene. Science 284(5412), 321-5 (1999).

Li, Q., Karam, S.M., Coerver, K.A., Matzuk M.M., and Gordon, J.I. Stimulation of activin receptor II signaling pathways inhibits differentiation of multiple gastric epithelial lineages. Mol Endocrinol. 12(2), 181-192(1998).

Li, Q., Karam, S.M., and Gordon, J.I. Diphtheria toxin-mediated ablation of parietal cells in the stomach of transgenic mice. J. Biol. Chem. 271, 3671-3676 (1996).

Li, Q., Karam, S.M., and Gordon, J.I. Simian virus 40 T antigen-induced amplification of pre-parietal cells in transgenic mice: effects on other gastric epithelial cell lineages and evidence for a p53-independent apoptotic mechanism that operates in a committed progenitor. J. Biol. Chem. 270, 15777-15788 (1995).

Li, Q., Kay, M.A., Finegold, M. Stratford-Pericaudet, L.D., and Woo, S. Assessment of recombinant adenoviral vectors for hepatic gene therapy. Human Gene Therapy 4, 403-409 (1993).

Education

Peking Univ, Beijing, China, B.S. Biology 1987

Peking Univ, Beijing, China, MS, Genetics 1990

Washington Univ, St. Louis MO, Ph.D. Molecular Cell Biology 1997
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