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. 2020 Jan 23;21(3):753. doi: 10.3390/ijms21030753

Figure 1.

Figure 1

Physiological and rearranged NTRK genes/TRK receptors and intracellular signaling. The PLC-γ, MAPK, and PI3-K intracellular pathways (here represented by the DAG/IP3, RAS/MEK/ERK, and PI3-K/AKT components, respectively) are activated either from the wild-type form of NTRK, and the chimeric fusion receptors (e.g., BCAN-NTRK1 and ETV6-NTRK3). However, the latter happens in a ligand-free constitutively activated fashion, leading to oncogenic activation. The NTRK inhibitors (TKI, here represented by entrectinib and larotrectinib) achieve their antitumor activity by interacting with the intracellular domain of the chimeric receptors, inhibiting the recruitment of the signaling pathway.