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Research in Liang Lab

We have for the first time identified UVRAG (UV Radiation Resistance Associate Gene) as a robust autophagy activator and tumor suppressor. Using cutting-edge technology including proteomic study, confocal/live cell imaging, cell culture and murine models, we have been able to demonstrate the roles for UVRAG in autophagy pathway, in membrane trafficking, and in tumor development (refer to NCB 2006 8(7): 688-699; NCB 2008 10(7): 759-61; Current Opinion in cell biology 2010 22(2): 226-33). We will continue to probe the underlying mechanism of UVRAG-mediated autophagy and genomic stability in tumor growth and response to cancer therapy.

Furthermore, we have established that the viral Bcl-2 (vBcl-2) of the γ-Herpesviruses (γ-HVs) family suppresses autophagy by directly targeting a key autophagy effector protein, Beclin1, and that vBcl-2s of γ-HVs has evolved enhanced anti-autophagic activity when compared to their host counterpart (PLoS Pathogen 2009 5(10)). We have investigated the functional significance and distinct contribution of virus-mediated autophagy and apoptosis inhibition in viral virulence. Rigorous efforts will continue to further explore the complex interaction between cells’ homeostatic and safeguard processes and viral entry, infection, and pathogenesis. believe our studies will not only unravel the molecular basis of ‘day job’ of important cellular process, but also help translate these information to more effective cancer therapy and infection control.

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