Qiutang Li, Ph.D.
301 E. Muhammad Ali Boulevard, Louisville KY 40202
Telephone: 502-852-2409 Fax: 502-852-6909
Washington Univ, St. Louis MO - 1997
Peking Univ, Beijing, China - 1990
Peking Univ, Beijing, China - 1987
My laboratory is interested in the study of two signal transduction pathways, i.e., 14-3-3sigma mediated and NF-κB pathways. 14-3-3sigma, functioning as a tumor suppressor protein, regulates normal epithelial development and differentiation, including daily renewing of the corneal epithelial cells. NF-κBs are transcription factors controlling a large number of genes involved in cell apoptosis, survival and inflammation.
As the most anterior part of eye, the cornea is indispensable for normal vision. More than forty-five millions of individuals worldwide are bilaterally blind and another 135 million have severely impaired vision in both eyes due to corneal opacity. Our research is focused on the role of 14-3-3sigma in epithelial development, homeostasis, wound healing, and tumorigenesis. We are currently investigating the molecular and functional roles of 14-3-3-sigma in corneal epithelium development and wound healing process by using the 14-3-3sigma mutant mice as animal model. We are also interested in elucidation of the molecular mechanism for development of corneal diseases, such as corneal intraepithelial neoplasia and squamous cell carcinoma; and providing new strategies for diagnosis and treatment.
It is well known that increased activation of NF-κB induces excessive inflammatory responses. Over activation of NF-κB plays critical role in initiation and development of cardiovascular or neurological degeneration diseases, as well as some types of cancers. Although the NF-κB has been postulated as a risk inflammatory factor in multiple eye diseases such as uveitis and AMD, the molecular mechanism has not been elucidated in detail. We aim to investigate the functional role of NF-κB in ocular tissues and the impact of NF-κB deletion in development of a variety of ocular diseases, using NF-κB gene knockout mouse models. Our investigation targets to search for novel therapeutic approaches for treating eye diseases
PUBLICATIONS: (15 selected publications from 23)
- Xin Y, Lu Q, Li Q. 14-3-3sigma controls corneal epithelial cell proliferation and differentiation through the Notch signaling pathway. Biochem Biophys Res Commun. 19;392(4):593-8 (2010). PMID: 20100467.
- Xin Y, Lu Q, Li Q. 14-3-3σ is required for club hair retention. Journal of Investigative 130(7):1934-6 (2010). PMID: 20237493.
- Liu Y, Ye F, Li Q, Tamiya S, Darling DS, Kaplan HJ, Dean DC. Zeb1 represses Mitf and regulates pigment synthesis, cell proliferation, and epithelial morphology. Invest Ophthalmol Vis Sci. 50(11):5080-8 (2009). PMID: 19515996.
- 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). PMID: 16239341.
- Gustin JA, Korgaonkar CK, Pincheira R, Li Q, Donner DB. Akt regulates basal and induced processing of NF-kB2 (p100) to p52. J Biol Chem. 281(24):16473-81. (2006). PMID: 16613850.
- Li Q, Lu Q, Bottero V, Estepa G, Morrison L, Mercurio F and Verma IM. Enhanced NF-κB activation and cellular function in macrophages lacking IκB kinase 1 (IKK1). PNAS 102(35):12425-30. (2005). PMID: 16116086.
- Li Q, Withoff S, and Verma IM. Inflammation-associated cancer: NF-kB is the lynchpin. Trends Immunol. 26(6):318-25.(2005). PMID: 15922948. Review
- Li Q, Verma IM. NF-kappaB regulation in the immune system. Nat Rev Immunol. 2(10):725-34(2002). PMID: 12360211. Review
- Li Q, Estepa G., Memet S., Israel A., and Verma IM. Complete lack of NF-κB activity in IKK1 and IKK2 double deficient mice: Additional defect in neurulation. Genes Dev. 14(14):1729-33 (2000). PMID: 10898787.
- 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). PMID: 10346820.
- 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). PMID: 10195897.
- 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). PMID: 9482661.
- 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). PMID: 8631979.
- 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). PMID: 7797580.
- 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). PMID: 8399487.