Tropomyosin receptor kinase C

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Protein NTRK3 PDB 1wwc

Tropomyosin receptor kinase C (TrkC), also known as NT-3 growth factor receptor, is a protein that in humans is encoded by the NTRK3 gene. TrkC is a member of the tropomyosin receptor kinase (Trk) family of tyrosine kinase receptors, which are key regulators in the development and maintenance of the nervous system. TrkC specifically binds to and is activated by neurotrophin-3 (NT-3).

Function[edit | edit source]

TrkC plays a critical role in the development and function of the nervous system. It is involved in the differentiation and survival of certain neuronal populations during development. Upon binding with its ligand, NT-3, TrkC dimerizes and undergoes autophosphorylation, which activates its kinase activity. This activation leads to the phosphorylation of downstream signaling molecules and the activation of signaling pathways that promote neuronal survival, growth, and differentiation.

Structure[edit | edit source]

The structure of TrkC includes an extracellular domain, which binds to NT-3, a single transmembrane domain, and an intracellular domain that contains the tyrosine kinase activity. The extracellular domain consists of several leucine-rich repeats and cysteine clusters, which are characteristic of the Trk family of receptors.

Clinical Significance[edit | edit source]

Alterations in the expression or function of TrkC have been implicated in various neurological disorders and diseases. Overexpression of TrkC has been observed in certain types of cancer, suggesting a potential role in tumorigenesis. Conversely, loss of TrkC function may contribute to neurodegenerative diseases due to the reduced survival of neurons that depend on NT-3/TrkC signaling.

Research[edit | edit source]

Research on TrkC has focused on understanding its role in the nervous system and exploring its potential as a therapeutic target in neurological disorders and cancer. Studies have investigated the use of TrkC agonists or NT-3 mimetics to promote neuronal survival and regeneration in various models of neurodegenerative diseases. Additionally, inhibitors of TrkC kinase activity are being explored for their potential to inhibit the growth of TrkC-expressing tumors.

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Contributors: Prab R. Tumpati, MD