1. Omics Types

oxidative phosphorylation

Definition

Oxidative phosphorylation is the metabolic pathway in which cells use enzymes to oxidize nutrients, thereby releasing chemical energy to produce adenosine triphosphate (ATP). This process occurs in the mitochondrial inner membrane and involves the electron transport chain (ETC) and ATP synthase. Electrons from NADH and FADH2 are transferred through protein complexes (I-IV), creating a proton gradient that drives ATP synthesis. Oxidative phosphorylation is the primary energy-generating pathway in aerobic organisms, producing approximately 30-32 ATP molecules per glucose molecule. Dysfunction in this pathway is implicated in mitochondrial diseases, neurodegenerative disorders, cancer metabolism, and aging. In metabolomics studies, oxidative phosphorylation activity is assessed by measuring metabolite levels, oxygen consumption rates, and ATP production.

Visualize oxidative phosphorylation in Nodes Bio

Researchers can visualize oxidative phosphorylation networks by mapping metabolite-enzyme-gene relationships across the electron transport chain. Nodes Bio enables integration of metabolomics data with transcriptomics and proteomics to identify bottlenecks in ATP production. Users can create interactive networks showing how metabolic perturbations propagate through Complex I-IV, visualize substrate-product relationships, and perform pathway enrichment analysis to understand mitochondrial dysfunction in disease contexts.

Visualization Ideas:

  • Electron transport chain complex interaction networks showing protein-metabolite relationships
  • Multi-omics integration networks connecting oxidative phosphorylation genes, proteins, and metabolites
  • Comparative pathway networks showing oxidative phosphorylation dysfunction across disease states or drug treatments
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Example Use Case

A pharmaceutical team investigating mitochondrial toxicity of drug candidates uses metabolomics to profile cellular energy metabolism. They measure metabolites including NADH, succinate, fumarate, and ATP levels in treated versus control cells. By visualizing oxidative phosphorylation networks in Nodes Bio, they identify that their lead compound inhibits Complex III, causing succinate accumulation and reduced ATP production. The network analysis reveals compensatory activation of glycolysis and helps predict off-target effects, guiding medicinal chemistry efforts to improve the compound's mitochondrial safety profile.

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