Data show that 5-Aza-dc reversed the alcohol-induced downregulation of neurotrophin-3 (Ntf3) correspondingly the expression of its receptor-neurotrophic receptor tyrosine kinase 3 (TrkC) was reduced.
Neurotrophin 3 -triggered TrkC seems to provide apparently stronger than nerve growth factor -triggered TrkA signal for neurite elongation in differentiating PC12 cells.
Study suggests a role for genes responsible for neural plasticity (NTRK3 and BDNF) in the pathophysiology of depression emphasizing hemispheric asymmetry in the level of gene expression
Data suggest that neurotrophins can promote cell viability through Trk receptors in a manner depending on basal neutral sphingomyelinase (nSMase) but not through SMase activity enhancement.
Transplantation of overexpressing neurotrophin-3-Schwann cells + trkC-neural stem cells in Gelfoam into the lesion gap immediately following injury results in significantly improved relay of the cortical motor evoked potential.
These results suggest that specific neurotrophins and trkA B and C receptors may contribute differentially to the survival and regenerative responses of extraocular motoneurons after lesion.
After nerve injury tyrosine kinase C expression is increased in small dorsal root ganglionic cells of allodynic animals and the medium- and large-size nonallodynic animals' cells.
PTPsigma can thus show differential complex formation with different Trk family members and in neurons can selectively target the neurite-forming signalling pathway driven by TrkA.
Runx3 determines TrkC positive sensory neuron identities through the transcriptional repression of TrkB when Trk-BTrkC double positive neurons differentiate into TrkC single positive neurons.
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