- ADJUNCT ASSISTANT PROFESSOR Oncological Sciences
B.S., Beijing Normal University
M.S., Beijing Normal University
Ph.D., Peking Union Medical College
Anatomy and Cell Biology
Mount Sinai School of Medicine
Molecular and Cell Biology
ResearchThe current project is focusing on investigating the function of Wnt signaling in the regulation of human bone biology as well as whether Wnt signaling can be a target in the therapeutic intervention of human bone-related disorders including bone tumors. The multi-potent mesenchymal stem cells (MSCs) originating from the adult human bone marrow has been used as model cells to study the function of Wnt signaling in bone differentiatin and regeneration. The lab is also focusing on identification of small molecules that can modulate Wnt signaling activity.
Liu XH, Kirschenbaum A, Yao S, Liu G, Aaronson SA, Levine AC. Androgen-induced Wnt signaling in preosteoblasts promotes the growth of MDA-PCa-2b human prostate cancer cells. Cancer Res 2007; 67(12): 5747-5753.
Liu G, Bafico A, Aaronson SA. The mechanism of endogenous receptor activation functionally distinguishes prototype canonical and noncanonical Wnts. Molecular Cell Biology 2005; 25(9): 3475-3482.
Bafico A, Liu G, Goldin L, Harris V, Aaronson SA. An autocrine mechanism for constitutive Wnt pathway activation in human cancer cells. Cancer Cell 2004; 6: 497-506.
Golan T, Yaniv A, Bafico A, Liu G, Gazit A. The human Frizzled 6 (HFz6) acts as a negative regulator of the canonical Wnt. beta-catenin signaling cascade. J Biol Chem 2004; 279(15): 14879-14888.
Liu G, Bafico A, Harris VK, Aaronson SA. A Novel Mechanism for Wnt activation of canonical signaling through LRP6 receptor. Molecular Cell Biology 2003; 23(16): 5825-5835.
Fang L, Li G, Liu G, Lee SW, Aaronson SA. p53 induction of heparin-binding EGF-like growth factor counteract p53 growth suppression through activation of MAPK and PI3K/Akt signaling cascades. EMBO J 2001; 20: 1931-1939.
Bafico A, Liu G, Yaniv A, Gazit A, Aaronson SA. Novel mechanism of Wnt signalling inhibition mediated by Dickkopf-1 interaction with LRP6/Arrow. Nature Cell Biology 2001; 3: 683-686.
Liu G, Wu M, Levi G, Ferrari N. Down-regulation of the Diphthamide biosynthesis protein 2-like gene during retinoid-induced differentiation and apoptosis: implications against its tumor-suppressor activity. International J. Cancer 2000; 88(3): 356-362.
Liu G, Wu M, Levi G, Ferrari N. Growth inhibition of human cancer cells by all-trans retinoic acid and N-(4-hydroxyphenyl) retinamide: a possible mechanism via regulation of retinoids receptors. International J. Cancer 1998; 78: 248-254.
Physicians and scientists on the faculty of the Icahn School of Medicine at Mount Sinai often interact with pharmaceutical, device and biotechnology companies to improve patient care, develop new therapies and achieve scientific breakthroughs. In order to promote an ethical and transparent environment for conducting research, providing clinical care and teaching, Mount Sinai requires that salaried faculty inform the School of their relationships with such companies.
Dr.Liu is not currently required to report Industry relationships.
Mount Sinai's faculty policies relating to faculty collaboration with industry are posted on our website at http://icahn.mssm.edu/about-us/services-and-resources/faculty-resources/handbooks-and-policies/faculty-handbook. Patients may wish to ask their physician about the activities they perform for companies.
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