I joined Cincinnati Children’s Hospital Medical Center in 2002 after training as a molecular and cellular biologist. I have an extensive background and long-term interest in immunology. Currently, I investigate the role and mechanisms of Rho family GTPases in T lymphocyte development and function.
Since beginning my work, I helped discover the role of Rho GTPases in T lymphocyte metabolism, which is important for T lymphocyte-mediated autoimmunity and allergy. Also, I helped determine the role of Rho family GTPases in anti-tumor T cell immunity.
My research has consistently been supported by National Institutes of Health (NIH) awards. I am also a reviewer of NIH grants for others’ research projects.
BS: Jilin University, Changchun, Jilin, China, 1994.
MS: Academy of Military Medical Sciences, Beijing, China, 1997.
PhD: Southern Medical University, Guangzhou, Guangdong, China, 2000.
Postdoctoral Research Associate: University of Tennessee, Memphis, TN, 2000-2002; Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, 2002-2004.
Research Associate: Southern Medical University, Guangzhou, Guangdong, China, 2000; Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, 2004.
Research Instructor: Cincinnati Children’s Hospital Medical Center, Cincinnati, OH. 2005-2009.
Rho GTPases and T and B lymphocyte development and function
Experimental Hematology and Cancer Biology, Cancer and Blood Diseases
Sensors and Devices Guided by Artificial Intelligence for Personalized Pain Medicine. Cyborg and Bionic Systems. 2024; 5:0160.
Efficacy and advantage of immunotherapy for melanoma via intramuscular co-expression of plasmid-encoded PD-1 and CTLA-4 scFvs. AMERICAN JOURNAL OF CANCER RESEARCH. 2024; 14:2626-2642.
Cdc42GAP deficiency contributes to the Alzheimer's disease phenotype. Brain: a journal of neurology. 2023; 146:4350-4365.
Kinase-independent role of mTOR and on-/off-target effects of an mTOR kinase inhibitor. Leukemia. 2023; 37:2073-2081.
Mechanism of inert inflammation in an immune checkpoint blockade-resistant tumor subtype bearing transcription elongation defects. Cell Reports. 2023; 42:112364.
Cdc42 signaling regulated by dopamine D2 receptor correlatively links specific brain regions of hippocampus to cocaine addiction. Biochimica et Biophysica Acta (BBA): Molecular Basis of Disease. 2023; 1869:166569.
Targeting of Cdc42 GTPase in regulatory T cells unleashes antitumor T-cell immunity. Journal for ImmunoTherapy of Cancer. 2022; 10:e004806.
Tumors bearing defective transcription elongation are immune hot but resistant to immune checkpoint inhibitors. Journal of immunology (Baltimore, Md. : 1950). 2022; 208:119.11.
Regulation of Cdc42 signaling by the dopamine D2 receptor in a mouse model of Parkinson's disease. Aging Cell. 2022; 21:e13588.
Human Spinal Organoid-on-a-Chip to Model Nociceptive Circuitry for Pain Therapeutics Discovery. Analytical Chemistry. 2022; 94:1365-1372.