About

Research Area

The Wei group has been at the forefront of unraveling the molecular mechanisms underlying how aberrant cell signaling events such as phosphorylation, ubiquitination and acetylation of critical cell-fate regulators, as well as understanding the dynamic interplay between these important signaling pathways, contribute to aberrant cell cycle regulation and tumorigenesis. To this end, we have been using a multi-disciplinary approach, including biochemical, cellular and mice modeling approaches to provide mechanistic insights into the regulation and function of three key multi-component enzymatic complexes: APC, SCF, and mTOR, and how dysregulation of their activities contributes to cell cycle aberrancy and ultimately, tumorigenesis.

• Identification of novel downstream ubiquitin substrates for key E3 ligases including Fbw7 and b-TRCP and reveal their role in tumorigenesis
• Characterization of upstream regulatory mechanisms governing the E3 ligase and oncogenic activity of Skp2
• Exploration of E3 ligase-independent functions of Cdh1 and its role in cell cycle
• Expansion in our understanding for various regulatory mechanisms of key mTOR pathway components including mTORC2 and Akt.
• Recently we are interested in understanding how PD-L1 is aberrantly elevated in tumor cells to impact cellular response to checkpoint blockade immunotherapy.
• To understand how to better harness the power of PROTAC or DUBTAC as novel anti-cancer therapies.

Together, these studies provide the molecular basis for understanding how aberrant cell signaling events contribute to tumorigenesis, as well as offer the rationale to develop novel anti-cancer therapies targeting specific cell signaling pathways including ubiquitination and phosphorylation.