Upon ligand binding, TKRs undergo a conformational change that leads to dimerization and autophosphorylation of tyrosine residues within the intracellular kinase domain. This autophosphorylation creates docking sites for various signaling molecules, initiating a cascade of downstream signaling pathways such as the RAS/MAPK, PI3K/AKT, and the JAK/STAT pathways. These pathways ultimately result in altered gene expression and cellular responses.
