This kinase is a membrane-bound receptor that, upon neurotrophin binding, phosphorylates itself (autophosphorylation) and members of the MAPK pathway.

The presence of this kinase leads to cell differentiation and may play a role in specifying sensory neuron subtypes.

Mutations in this gene have been associated with congenital insensitivity to pain with anhidrosis, self-mutilating behaviors, intellectual disability and/or cognitive impairment and certain cancers.

[7] TrkA is the high affinity catalytic receptor for the neurotrophin, Nerve Growth Factor, or "NGF".

As a kinase, TrkA mediates the multiple effects of NGF, which include neuronal differentiation, neural proliferation, nociceptor response, and avoidance of programmed cell death.

[9] This interaction leads to a cross linking dimeric complex where parts of the ligand-binding domains on TrkA are associated with their respective ligands.

[10] After being immediately bound by NGF, the NGF/TrkA complex is brought from the synapse to the cell body through endocytosis where it then activates the NGF-dependent transcriptional program.

[14] Thus, Trk is the mediator of developmental and growth processes of NGF, and plays a critical role in the development of the nervous system in many organisms.

[15] In one study done on patients with functional dyspepsia, scientists found a significant increase in TrkA and nerve growth factor in gastric mucosa.

[16] In one study, a total absence of TrkA receptor was found in keratoconus-affected corneas, along with an increased level of repressor isoform of Sp3 transcription factor.

[18] In a research study by Vaishnavi A. et al., NTRK1 fusions are estimated to occur in 3.3% of lung cancer as assessed through next generation sequencing or fluorescence in situ hybridization.