kinome
Definition
The kinome represents the complete set of protein kinases encoded by an organism's genome. In humans, this comprises approximately 518 kinases that catalyze phosphorylation reactions, transferring phosphate groups from ATP to specific substrates. Kinases are critical regulators of cellular signaling pathways, controlling processes including cell growth, differentiation, metabolism, and apoptosis. The kinome is organized into families based on sequence similarity and catalytic domain structure, with major groups including tyrosine kinases, serine/threonine kinases, and lipid kinases. Understanding kinome activity and dysregulation is essential for disease research, particularly in cancer where aberrant kinase signaling drives oncogenesis. Kinome profiling techniques enable comprehensive analysis of kinase expression, activity, and drug interactions across biological systems.
Visualize kinome in Nodes Bio
Researchers can visualize kinome networks in Nodes Bio to map kinase-substrate relationships, identify signaling cascades, and analyze pathway crosstalk. Network graphs reveal how kinase families interconnect, highlighting central regulatory hubs and potential therapeutic targets. Users can overlay phosphoproteomics data to identify activated kinases in disease states, integrate drug-kinase interaction data to predict off-target effects, and perform pathway enrichment analysis to understand kinome-driven biological processes.
Visualization Ideas:
- Kinase-substrate interaction networks showing phosphorylation cascades
- Drug-kinome selectivity profiles mapping inhibitor binding across kinase families
- Disease-associated kinome rewiring networks comparing healthy versus pathological signaling states
Example Use Case
A pharmaceutical team developing a selective kinase inhibitor for melanoma uses kinome network analysis to assess drug specificity. They map their compound's binding profile across 300 kinases, visualizing interaction networks to identify primary targets (BRAF, MEK) and potential off-targets. By integrating patient phosphoproteomics data, they discover that resistant tumors activate compensatory kinase pathways involving EGFR and SRC family kinases. Network analysis reveals these escape mechanisms share common downstream effectors, suggesting rational combination therapy strategies to overcome resistance.