amino acid metabolism
Definition
Amino acid metabolism encompasses the biochemical pathways involved in the synthesis, degradation, and interconversion of amino acids within cells and organisms. This includes essential processes such as transamination, deamination, the urea cycle, and biosynthetic pathways for both proteinogenic and non-proteinogenic amino acids. Amino acid metabolism is critical for protein synthesis, energy production, neurotransmitter biosynthesis, and maintaining nitrogen balance. Dysregulation of these pathways is implicated in numerous diseases including metabolic disorders, cancer, neurological conditions, and inborn errors of metabolism. Metabolomic profiling of amino acids provides insights into cellular metabolic state, nutritional status, and disease progression.
Visualize amino acid metabolism in Nodes Bio
Researchers can use Nodes Bio to visualize amino acid metabolic networks, mapping relationships between amino acids, enzymes, transporters, and regulatory genes. Network analysis reveals metabolic bottlenecks, identifies key regulatory nodes, and integrates multi-omics data to understand how genetic variations or drug treatments affect amino acid flux. Pathway enrichment and causal inference tools help identify upstream regulators and downstream consequences of metabolic perturbations.
Visualization Ideas:
- Metabolic pathway networks showing enzyme-substrate relationships and flux directionality
- Multi-omics integration networks connecting amino acid levels with gene expression and protein abundance
- Disease-specific perturbation networks comparing healthy versus pathological amino acid metabolism states
Example Use Case
A cancer research team investigating glutamine addiction in tumor cells uses metabolomic profiling to measure amino acid levels across treatment conditions. They discover elevated glutamate and decreased asparagine levels following glutaminase inhibitor treatment. Using network visualization, they map the interconnected pathways of glutamine, glutamate, aspartate, and asparagine metabolism, identifying compensatory metabolic rewiring through asparagine synthetase upregulation. This reveals a potential resistance mechanism and suggests combination therapy targeting both glutaminase and asparagine synthetase to improve treatment efficacy.