Fig. 1 | npj Systems Biology and Applications

Fig. 1

From: Mechanistically detailed systems biology modeling of the HGF/Met pathway in hepatocellular carcinoma

Fig. 1

Diagram of the main molecular interactions implemented in the model. The diagram illustrates surface molecules and their interactions (on the left), as well as the intracellular downstream signaling to ERK (extracellular-regulated kinase) and Akt (on the right). Surface Met can bind hepatocyte growth factor (HGF) and get activated in the absence of α5β1 integrin that leads to rapid internalization and degradation, whereas integrin-bound Met has lower internalization/degradation and higher recycling rates. In addition to integrin-binding peptide (AXT050) that dissociates the Met/α5β1 complex, effect of anti-Met (cabozantinib), anti-HGF (rilotumumab), and Raf inhibitor (sorafenib) drugs were explored in this study

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