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St. Jude Children’s Research Hospital
PhD, University of Tennessee Medical School, 1996
The long-term interest of my lab is to understand how T-cell development and activations are regulated. My current study is focused on studying the role of two proteins involved in regulating T-cell development and functions: phospholipase C-γ (PLCγ) and B cell lymphoma 10 (Bcl10). PLCγ activation is one of the key events following TCR stimulation.
There are two PLCγ isoforms, PLCγ1 and PLCγ2. We have shown that PLCγ1 deficiency at late T-cell developmental stage impaired T-cell positive and negative selection, affected mature T-cell development and function, and resulted in T-cell lymphopenia and autoimmune diseases. Recently, we have also shown that PLCγ1 and PLCγ2 play an additive role in TCR signal transduction. Currently, we are studying the role of PLCγ1 and PLCγ2 in early T-cell lymphopoiesis and performing structural functional study of PLCγ1 and PLCγ2 in T-cell system.
Bcl10 gene is an adaptor protein cloned from the recurrent 1p22 breakpoint of chromosomal translocation t(1;14)(p22;q32) involved in mucosa associated lymphoid tissue (MALT) lymphoma. This translocation resulted in high-level expression of Bcl10 in MALT lymphoma with the t(1;14)(p22;q32). Therefore, high expression of Bcl10 is a potential mechanism for MALT lymphoma development. Bcl10 functions in TCR signaling downstream of PLCγ1, and is essential for TCR-mediated nuclear factor kappa B (NF-κB) activation, aberrant activation of which is associated with tumor development. Bcl10 deficiency impaired T-cell development, proliferation and interleukine-2 production. We have demonstrated that TCR-induced phosphorylation of Bcl10 is a mechanism of downregulating Bcl10 protein level and thus terminating TCR-mediated NF-κB activation. Currently, we are further studying the mechanism on how phosphorylation of Bcl10 affects its function in TCR signal transduction.
Sr. Research Associate