My clinical interests are in the area of chronic pain following injury and disease. Research focuses on recovery from chronic pain and sensory abnormalities following central and peripheral nervous system injury.
- Molecular and cellular mechanisms involved in pain/sensory dysfunction following spinal cord injury
- Neuroprotective effect of exercise in recovery from chronic pain and improved cognitive function following central nervous system injury
Masters in Physical Therapy
Ph.D. Anatomy and Cell Biology
East Carolina University
S. K. Bareiss and Q. Lu. δ-Catenin: A new member of the glycogen synthase kinase-3b signaling complex that promotes b-catenin turnover in neurons. Journal of Neuroscience Research, 2010 Aug 15; 88(11):2350-63.
M. Oh, H. Kim, I. Yang, J. Park, W. Cong, M. Baek, S. K. Bareiss, H. Ki, Q. Lu, J. No, I. Kwon, J. Choi, and K. Kim , GSK-3 phosphorylates δ-catenin and negatively regulates its stability via ubiquitination/proteosome-mediated proteolysis. Journal of Biological Chemistry, 2009 Oct 16; 284(42): 28579-89.
K. Kwonseop, M. Oh, H. Ki, T. Wang, S. Bareiss, M. Fini, D. Li, and Q. Lu, Identification of E2F1 as a positive transcriptional regulator for d-catenin, Biochemical and Biophysical Research Communications, 2008 May 2; 369(2):414-20.
J. Kim*, S. K. Bareiss*, K. Kim, R. Tatum, J. Han, Y. Jin, H. Kim, Q. Lu, and K. Kim, Presenilin-1 inhibits δ-catenin-induced cellular branching and promotes δ-catenin processing and turnover. Biochemical and Biophysical Research Communications. 2006 Dec; 351(4):903-8.
Kristin Hernandez, Physical Therapy Doctoral Student
Tiffany Lee, Undergraduate ECU Neuroscience Student
Andrew McGowan, Undergraduate ECU Neuroscience Student