Ntrk3 Gene is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
:: infobox .infobox-gene
Symbol: NTRK3
Full Name: Neurotrophic Receptor Tyrosine Kinase 3
Chromosomal Location: 15q25.3
NCBI Gene ID: 4916
OMIM: 191316
Ensembl ID: ENSG00000140538
UniProt: Q9UIK5
Proteins: TrkC
Associated Diseases: Congenital Myopathy, Alzheimer's Disease
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NTKR3 is a gene/protein encoding a key neuronal protein involved in synaptic function, signal transduction, and cellular homeostasis. Dysfunction of NTKR3 is associated with neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, and related disorders.
NTRK3 encodes TrkC (Tropomyosin receptor kinase C), the primary receptor for neurotrophin-3 (NT-3). TrkC is a receptor tyrosine kinase important for neuronal development, particularly in sensory neuron differentiation and synaptic formation. While less studied in neurodegeneration than TrkA and TrkB, NT-3/TrkC signaling may have protective effects in the aging brain.
TrkC is expressed in:
- Hippocampus (CA1-CA3)
- Cerebral cortex (layers II-III, V)
- Basal forebrain cholinergic neurons
- Dorsal root ganglia
- Cerebellum (Purkinje cells)
- Substantia nigra
Expression in hippocampal and cortical regions suggests roles in synaptic plasticity.
- Lamballe F, et al. (1991). "The trkC tyrosine kinase: a receptor for neurotrophin-3." Cell. PMID:1846705
- Menn B, et al. (1998). "TrkC is expressed in hippocampal excitatory interneurons." J Comp Neurol. PMID:9721652
- Tessarollo L, et al. (1993). "TrkC is a functional receptor for NT-3." Dev Biol. PMID:8391756
The study of Ntrk3 Gene has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.
Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.
- Doebele RC et al.. "Entrectinib in patients with advanced or metastatic NTRK fusion-positive solid tumours: integrated analysis of three phase 1-2 trials." The Lancet. Oncology (2020). DOI: 10.1016/S1470-2045(19)30691-6 PubMed: 31838007
- Lu T et al.. "Decoding transcriptional identity in developing human sensory neurons and organoid modeling." Cell (2024). DOI: 10.1016/j.cell.2024.10.023 PubMed: 39536745
- Jiang T et al.. "Development of small-molecule tropomyosin receptor kinase (TRK) inhibitors for NTRK fusion cancers." Acta pharmaceutica Sinica. B (2021). DOI: 10.1016/j.apsb.2020.05.004 PubMed: 33643817
- Gianno F et al.. "Paediatric-type diffuse high-grade gliomas in the 5th CNS WHO Classification." Pathologica (2022). DOI: 10.32074/1591-951X-830 PubMed: 36534421
- Singh AK et al.. "Epigenetic modulation rescues neurodevelopmental deficits in Syngap1+/- mice." Aging cell (2025). DOI: 10.1111/acel.14408 PubMed: 39878322
- Manea CA et al.. "A review of NTRK fusions in cancer." Annals of medicine and surgery (2012) (2022). DOI: 10.1016/j.amsu.2022.103893 PubMed: 35860155
- Argani P, Ladanyi M. "Recent advances in pediatric renal neoplasia." Advances in anatomic pathology (2003). PubMed: 12973047
- Nurnberger JI et al.. "Identification of pathways for bipolar disorder: a meta-analysis." JAMA psychiatry (2014). DOI: 10.1001/jamapsychiatry.2014.176 PubMed: 24718920