TrkA Protein, Human (sf9, Flag, Avi)

TrkA Protein, a receptor tyrosine kinase, plays a crucial role in the development and maturation of both the central and peripheral nervous systems, exerting control over the proliferation, differentiation, and survival of sympathetic and sensory neurons. Functioning as a high-affinity receptor for NGF, its primary ligand, TrkA undergoes homodimerization, autophosphorylation, and activation upon dimeric NGF ligand-binding. This activation leads to the recruitment, phosphorylation, and/or activation of downstream effectors, including SHC1, FRS2, SH2B1, SH2B2, and PLCG1, orchestrating distinct signaling cascades that drive cell survival and differentiation. TrkA regulates diverse cellular processes through pathways such as the GRB2-Ras-MAPK cascade, Ras-PI3 kinase-AKT1 signaling, and NF-Kappa-B activation. In the absence of ligand and activation, TrkA may contribute to cell death, emphasizing the dependence of neuron survival on trophic factors. Interestingly, it exhibits resistance to NGF, constitutively activating AKT1 and NF-kappa-B, while unable to activate the Ras-MAPK signaling cascade. TrkA also antagonizes the anti-proliferative NGF-NTRK1 signaling, promoting neuronal precursor differentiation. The isoform TrkA-III additionally plays a role in angiogenesis and exhibits oncogenic activity upon overexpression.