B.S., East China Normal University
M.S., Emory University
Ph.D., Emory University
Postdoctoral Fellow, Harvard Medical School
Postdoctoral Fellow, Brigham and Women's Hospital

office: Brody 7N-72A
telephone: 252-744-2844
e-mail: luq@ecu.edu

| Research | Selected Publications | Staff and Students |

Research
My laboratory studies the molecular mechanisms of cellular injuries, which include toxicity induced neuronal degenerations as well as cellular damages during cancer formation. Currently, one project explores regulation of Rho family small GTPases in the anti-cancer drug induced neurodegeneration and regeneration. Another project employs the prostate cancer xenograft and its derived cell lines to investigate signaling through protein-protein interactions in the Rho GTPase pathway.

Axons and dendrites are the major components of polarized neurons. During neuronal injuries, many changes occur that impact the axon and dendrite morphology and function. Recent studies from my laboratory have shown that dendrite degeneration precedes the loss of cell viability. Studies also show that Rho family small GTPases and their regulatory elements play critical roles in the dendritic degenerative processes. One mechanism that mediates this regulation is the STI571/Glivec sensitive non-receptor tyrosine kinase Abl. Currently, primary neuronal cultures, high resolution time-lapse microscopic imaging, and GTPase activity assays are being used to determine the interactions between Rho GTPases and the Abl mediated upstream regulators, as well as between Rho GTPases and their downstream effectors. The project will help elucidate the mechanisms that control neuronal morphology and functions, and it will facilitate the identification of therapeutic targets in neural regeneration following injuries.

Proteins in the Rho GTPase signaling cascade also influence many aspects of tumorigenesis and cancer progression. Our recent studies have identified the upregulation of a RhoA inhibitory component in prostate cancer formation. Modified Ca25, a neural specific protein that is turned on in prostatic adenocarcinomas, can be excreted as aggregates. Pathway analysis will determine its regulation, leading to the validation of Ca25 as a potential cancer biomarker. Within the Rho GTPase cascade, Ca25 interacts with cadherin/catenin and catenin/IQGAP-1 systems. Currently, molecular and biochemical approaches are being employed to determine protein-protein interactions that will reveal how Ca25 regulates cell-cell adhesion in prostate cancer. This project will establish new diagnostic biomarkers for prostate cancer, and it will provide a better understanding of Rho GTPase regulation of cancer formation and progression.

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Selected Publications
Lu, Q. and J.G. Wood. 1993. Functional studies of Alzheimer's disease tau protein. J. Neurosci. 13:508-515.

Lu, Q., J.P. Soria, and J.G. Wood. 1993. p44mpk MAP kinase induces Alzheimer type alterations in tau function and in primary hippocampal neurons. J. Neurosci. Res. 35: 439-444.

Lu, Q., R. Kanumury, and J.G. Wood. 1994. Abnormal phosphorylation of tau proteins in brain microtubules: Activation by excess ATP and tyrosine dephosphorylation. J. Neurosci. Res. 37: 759-768.

Ferreira, A., Q. Lu, L. Orecchio, and K.S. Kosik. 1997. Selective phosphorylation of adult tau isoforms in mature hippocampal neurons exposed to fibrillar Aβ. Molec. Cell Neurosci. 9:220-234.

Lu, Q., M. Paredes, J.M. Zhang, and K.S. Kosik. 1998. Basal extracellular signal-regulated kinase activity modulates cell-cell and cell-matrix interactions. Molec. Cell Biol. 18: 3257-3265.

Lu, Q., M. Paredes, M. Medina, J.H. Zhou, L. Orecchio, and K.S. Kosik. 1999. δ-catenin: an adhesive junction associated protein which promotes motile behavior. J. Cell Biol. 144: 519-532.

Chen, Y.-H. and Q. Lu (equal contribution), E. Scheneeberg, and D. Goodenough. 2000. Restoration of junction assembly and barrier function by down regulation of MAP kinase pathway in ras-transformed MDCK cells. Molec. Biol. Cell 11: 849-862.

Lu Q., N. Mukhopadhyay, J. Griffin, M. Paredes, M. Medina, and K.S. Kosik. 2002. Brain armadillo protein δ-catenin interacts with Abl tyrosine kinase and modulates cellular morphogenesis in response to growth factors. J.Neurosci. Res. 67: 618-624.

Chen, Y.-H., Q. Lu, D.A. Goodenough, and B. Jeansonne. 2002. Non-receptor tyrosine kinase c-yes interacts with occludin during tight junction formation in canine kidney epithelial cells. Mol. Biol. Cell. 13: 1227-1237.

Jones, S.B., G.W. Lanford, Y.-H. Chen, M. Moribito, K. Kim, and Q. Lu. 2002. Glutamate-induced δ-catenin redistribution and dissociation from postsynaptic receptor complexes. Neuroscience. 115(4): 1009-1021.

Kim, K., A. Sirota, Y.-H. Chen, S. B. Jones, R. Dudek, G.W. Lanford, C. Thakore, and Q. Lu. 2002. Dendrite-like process formation and cytoskeletal remodeling regulated by δ-catenin expression. Exp. Cell Res. 275: 171-184.

Jones S.B., H.Y. Lu, and Q. Lu. 2004. Abl tyrosine kinase promotes dendrogenesis by inducing actin cytoskeletal rearrangements in cooperation with Rho family small GTPases in hippocampal neurons. J Neurosci. 24: 8510-8521.

Lu Q., L.J. Dobbs, C.W. Gregory, G.W. Lanford, M.P. Revelo, S. Shappell, and Y.-H. Chen. 2005. Increased expression of δ-catenin/neural plakophilin-related armadillo protein is associated with the down-regulation and redistribution of E-cadherin and p120ctn in human prostate cancer. Hum. Pathol. 36: 1037-1048.

Click PubMed Publications for further listings.

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Staff and Students
Location 7N-72

Former Students and Post-Doctoral Fellows:

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