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TrkC (Tropomyosin Receptor Kinase C) is a key member of the Trk family of neurotrophin receptors. Encoded by the *NTRK3* gene, this receptor tyrosine kinase primarily binds to its specific ligand, Neurotrophin-3 (NT-3). It is highly expressed in specific regions of both the central and peripheral nervous systems—particularly in proprioceptive neurons associated with motor coordination and balance, as well as in the cerebellum—where it plays a pivotal role in governing neuronal survival, differentiation, and synaptic plasticity.

The NT-3/TrkC signaling pathway serves as a central regulatory axis for the development and function of the nervous system. In this pathway, NT-3 acts as a specific ligand; upon binding to the receptor tyrosine kinase TrkC, it induces receptor dimerization and autophosphorylation. This process activates three key downstream signaling cascades—RAS/MAPK (proliferation/differentiation), PI3K/AKT (survival), and PLC-γ (plasticity)—which collectively mediate neuronal survival, differentiation, axonal growth, and synaptic plasticity, functions that are particularly critical for proprioception. Conversely, pathological activation of this pathway often stems from *NTRK3* gene fusions. Such fusions result in the constitutive, ligand-independent activation of the TrkC kinase domain, thereby transforming this physiological pathway—originally designed to sustain neuronal survival—into an oncogenic engine that drives the progression of various cancers. Consequently, this principle serves as the fundamental basis for the action of a broad spectrum of targeted therapeutic agents.

The TrkC Effector Reporter Cell model accurately simulates the *in vivo* signal transduction processes of TrkC; the underlying principle is illustrated in the figure below.

Figure 1. Schematic Diagram of the TRKC Effector Reporter Cell Model

Figure 2. Recombinant TRKC Effector Reporter Cell stably expressing TRKC.

Figure 3. Dose Response of Recombinant Human NT-3 in TRKC Effector Reporter Cell( C13).

Figure 4. Dose Response of TRKC Agonist Ab in TRKC Effector Reporter Cell( C13).

Figure 5. Inhibition of Human NT-3 induced Reporter Activity by NTRK Inhibitor in TRKC Effector Reporter Cell( C13).

Cell Resuscitation
1)Rapidly thaw the frozen cells in a 37 °C water bath for approximately 60 seconds. Once thawed (which may take slightly less or more than 60 seconds), immediately transfer the cell suspension from the cryovial into a 15 mL centrifuge tube containing 10 mL of pre-warmed  TRKC Effector Reporter Cell complete culture medium.
2)Centrifuge cells at 1000 rpm for 5 min to remove medium, then resuspend cells in 5 mL of pre-warmed complete medium.
3)Transfer the cell suspension into a T25 culture flask and incubate at 37 °C with 5% CO₂.
4)After approximately 24–36 hours, replace the medium or passage the cells to remove non-adherent dead cells.

Subculturing procedure
1)When the cell density reaches the appropriate confluency for passaging, wash the cells with PBS, then add 1 mL trypsin to detach the cells. When more than 80% of the cells detach upon gently tapping the culture flask, add complete culture medium to terminate digestion. Gently pipette to obtain a single-cell suspension, transfer to a 15 mL centrifuge tube, and centrifuge at 1000 rpm for 5 minutes.

2)Discard supernatant after centrifugation. Resuspend cells in fresh medium to a single-cell suspension and transfer to a new culture flask for continued growth.

Cell Freezing
After trypsinization and centrifugation of cells from each T75 flask or 10 cm culture dish, discard the supernatant. Add 2 mL of cryopreservation medium (90% FBS + 10% DMSO), gently resuspend thoroughly, and aliquot into two cryovials. Immediately place the cryovials into a controlled-rate freezing container (e.g., Nalgene 5100-0001), fill with isopropanol to the indicated level, and store at −80 °C. After 24 hours, transfer the cryovials to liquid nitrogen for long-term storage.