Research Paper Volume 16, Issue 7 pp 6588—6612
TGF-β downstream of Smad3 and MAPK signaling antagonistically regulate the viability and partial epithelial–mesenchymal transition of liver progenitor cells
Figure 9. Schematic illustration of this study. In LPCs, TGF-β activated Smad and MAPK signaling, and activated MAPK signaling contributed to linker phosphorylation of Smad3 at T179 and S213. TGF-β-activated Smad signaling contributes to the cytostasis and EMT of LPCs, whereas TGF-β-activated MAPK signaling and phosphorylation of Smad3 at T179 and S213 have opposite effects.