Address
Dept. Of Pharmacology
Creighton University School of Medicine
2500 California Plaza
Omaha, NE 68178

Nebraska Center for Cellular Signaling

Telephone: (402) 280-2173
Fax: (402) 280-2142
Email: yat60399@creighton.edu  

Education:

• B.S. Wuhan University, China
• Ph.D. National Laboratory of Biomacromolecules, Institute of Biophysics, Academia Sinica, Beijing , China

• My research focuses on the regulation of the interaction among G protein coupled receptor (GPCR), G proteins and RGS (Regulators of G Protein Signaling) proteins in cardiovascular disease and prostate cancer. GPCR/G protein-mediated signaling controls many cellular processes. G proteins stimulate intracellular signaling proteins (effectors) when they bind GTP in response to receptor; signaling ends when bound GTP is hydrolyzed. RGS proteins can act as GTPase-Activating Proteins (GAPs) and may accelerate the deactivation of G proteins by 1000-fold. It is important to understand how RGS proteins can act as tightly regulated modulators and integrators of multiple GPCR/G protein signaling pathways. This elucidation will not only help us understand the roles RGS proteins play in physiology and diseases, but has the potential to provide crucial information for RGS-target drug development.

• P20 RR018759 M.J. Wheelock (PI) 7/1/2003-6/30/2008 National Institutes of Health; Title: Nebraska Center for Cellular Signaling Project Leader: Yaping Tu 7/1/2004-6/30/2007 GPCR Signaling and Prostate Cancer Development and Progression The overall goal of this proposal is to provide evidence for a cause-and-effect relationship between dysregulated GPCR signaling and androgen-independent growth of prostate cancer cells both in culture and in athymic nude mice.
• Nebraska State LB692 Tu (PI) 10/1/2004-9/30/2006 Tobacco Settlement Funds Molecular Mechanism of Galpha12 in Androgen-independent Prostate Cancer” This study investigates the roles of Galpha12 and its specific RGS protein (LARG) in androgen-independent prostate cancer cell migration and invasion.

• Cao, X., Qin, J., Xie, Y., Khan, O., Dowd, F., Scofield, M., Lin, M.F. and Tu, Y. (2006) "Regulator of G-protein Signaling 2 (RGS2) inhibits androgen-independent activation of androgen receptor in prostate cancer cells", Oncogene 25: 3719-3734
• Tang, W., Tu, Y., Nayak, S.K., Woodson, J., Jehl, M., and Ross, E.M. (2006) Gβγ inhibits Gα GTPase- Activating Proteins (GAPs) by inhibition of G?-GTP binding during stimulation by receptor, J. Biol. Chem. 281: 4746-4753
• Khan, O., Fu, G., Ismail, A., Srinivasan, S., Cao, X., Tu, Y., Lu, S. and Nawaz, Z. (2006) "Multifunction steroid receptor coactivator, E6-associated protein, E6-AP is involved in development of the prostate gland" Mol. Endocrinol. 20: 544-559.
• Tu, Y. and Wilkie, T.M. (2004) Allosteric Regulation of RGS Domain GAP Activity, Methods Enzymol. 389: 89-105.
• Tu, Y., Nayak, S. K., Woodson, J. and Ross, E. M. (2003) Phosphorylation-Regulated Inhibition of the Gz GAP Activity of RGS Proteins by Synapsin Ia, J. Biol. Chem. 278: 52273-52281.
• Ouyang, Y.S. Tu, Y. and Yang, F.Y. (2003) The mutation in the N-terminal domain of RGS4 disrupts PA-conferred inhibitory effect on GAP activity, Biosci Rep 23: 213-224.
• Ouyang, Y.S. Tu, Y., Barker,S.A. and Yang, F.Y. (2003) RGS4: Insertion into Model Membranes and Inhibition of Activity by Phosphatidic Acid, J. Biol. Chem., 278: 11115-11122.
• Tu, Y., Woodson, J. and Ross, E.M. (2001) Binding of Regulator of G Protein Signaling (RGS) Proteins to Phospholipid Bilayers. Contribution of Location and/ or Orientation to GTPase-activating Protein Activity, J. Biol. Chem., 276: 20160-20166.