receptor tyrosine kinase
Definition
Receptor tyrosine kinases (RTKs) are transmembrane proteins that initiate intracellular signaling cascades upon binding extracellular ligands such as growth factors, hormones, or cytokines. Upon ligand binding, RTKs undergo dimerization and autophosphorylation of tyrosine residues on their intracellular domains, creating docking sites for adaptor proteins and enzymes. This triggers downstream signaling through pathways including RAS/MAPK, PI3K/AKT, and JAK/STAT, regulating cell proliferation, differentiation, survival, and metabolism. RTKs include families such as EGFR, VEGFR, PDGFR, and insulin receptor. Dysregulation through mutations, overexpression, or aberrant activation drives many cancers and developmental disorders, making RTKs critical therapeutic targets. Understanding RTK signaling networks is essential for drug development and precision medicine approaches.
Visualize receptor tyrosine kinase in Nodes Bio
Researchers can map RTK signaling cascades as hierarchical networks, visualizing ligand-receptor interactions, phosphorylation events, and downstream effector pathways. Nodes Bio enables analysis of crosstalk between multiple RTK pathways, identification of feedback loops, and exploration of how mutations alter network topology. Users can overlay expression data, drug targets, or disease associations to identify key regulatory nodes and predict therapeutic intervention points in complex signaling networks.
Visualization Ideas:
- Ligand-receptor-effector cascade networks showing signal flow from RTK activation to transcriptional responses
- Multi-pathway crosstalk maps comparing parallel RTK signaling routes and convergence points
- Drug target networks displaying RTK inhibitors, their binding sites, and affected downstream signaling nodes
Example Use Case
An oncology research team investigating resistance to EGFR inhibitors in lung cancer uses network visualization to map compensatory RTK signaling. They construct a network showing EGFR, MET, and HER2 pathways with their downstream effectors. By overlaying phosphoproteomic data from resistant cell lines, they identify MET receptor amplification creating an alternative activation route to the MAPK pathway. The network reveals that dual inhibition of EGFR and MET converges on critical nodes like ERK, suggesting a combination therapy strategy that their subsequent experiments validate.