These conserved tyrosine serve as docking sites for adaptor proteins that trigger downstream signaling cascades.

Signaling through PLCG1, PI3K and RAAS, downstream of activated NTRK3, regulates cell survival, proliferation and motility[7] Moreover, TrkC has been identified as a novel synaptogenic adhesion molecule responsible for excitatory synapse development.

[9] NT-3 activation of catalytic TrkC isoform promotes both proliferation of neural crest cells and neuronal differentiation.

[citation needed] It has been demonstrated that NTRK3 is a dependence receptor, meaning that it can be capable of inducing proliferation when it binds to its ligand NT-3, however, the absence of the NT-3 will result in the induction of apoptosis by NTRK3.

These mice have normal nociception, but they are defective in proprioception, the sensory activity responsible for localizing the limbs in space.

[23] The promoter region of NTRK3 contains a dense CpG island located relatively adjacent to the transcription start site (TSS).

Using HumanMethylation450 arrays, quantitative methylation-specific PCR (qMSP), and Methylight assays, it has been indicated that NTRK3 is methylated in all CRC cell lines and non of the normal epithelium samples.

[24] It has also been suggested that methylation status of NTRK3 promoter is capable of discriminating CRC tumor samples from normal adjacent tumor-free tissue.

In vitro, entrectinib inhibits the Trk family members TrkA, TrkB and TrkC at low nano molar concentrations.

[39] Posterior studies, have shown that peptidomimetics with an organic backbone, and a pharmacophore based on β-turn NT-3 structure can also function as an antagonist of TrkC.