A linkage of Gαi2 and TGF-β signaling via a newly discovered Smad phosphatase

We have shown that TGF-β requires Gαi2 signaling to mediate its inhibitory effects on T cell proliferation and cytokine production.  The absence of Gαi2 resulted in accumulation of a Smad phosphatase PPM1A in the nucleus of T cells, which terminates TGF-β signaling prematurely, and renders T cells unresponsive to TGF-β.  We are elucidating how Gαi2 signaling regulates the stability of the Smad phosphatase. 

In light of the importance of TGF-β signaling in modulation of mucosal immune responses, the study would undoubtedly provide novel insights into the regulation of the TGF-β signaling.

Projects

• Suppression of Th17 differentiation by IEX-1
• IEX-1 can be a potential target for prevention of colitis and colon cancer
• Hypertension onset independent of inflammation
• Laser vaccine adjuvant effects
• A complex interaction between Gαi2 and Gαi3
• A linkage of Gαi2 and TGF-β signaling via a newly discovered Smad phosphatase