This study integrates transcriptomic, proteomic, and metabolomic analyses to determine hypoxia adaptation mechanisms.
First-pass extracted concept
integrated transcriptomic, proteomic, and metabolomic analysis
Candidate: concept label1 source documents4 linked claims
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Aliases
multi-omics analysis
Evidence Snippets
Supporting Sources
Linked Claims
Cross-omics integration identified 37 shared pathways, including VEGF, GnRH, and C-type lectin receptor signaling pathways co-regulated at the transcriptomic-metabolomic level.
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Cross-omics integration uncovered 37 shared pathways, with VEGF, GnRH, and C-type lectin receptor signaling pathways being co-regulated at the transcriptomic-metabolomic level.
Metabolomic profiling revealed 463 differential metabolites associated mainly with glycerophospholipid metabolism, arachidonic acid metabolism, and VEGF signaling.
Quoted textsource-backed
Metabolomic profiling revealed 463 differential metabolites, predominantly associated with glycerophospholipid metabolism, arachidonic acid metabolism, and VEGF signaling.
Proteomic screening detected 388 differentially abundant proteins, with unique enrichment in the cytokine-cytokine receptor interaction pathway.
Quoted textsource-backed
Proteomic screening detected 388 differentially abundant proteins, uniquely enriched in the cytokine-cytokine receptor interaction pathway.
Transcriptomic analysis identified 852 differentially expressed genes in the hypoxia comparison, with enrichment in hypoxia-inducible factor signaling, glycolysis/gluconeogenesis, and IL-17-mediated immunity.
Quoted textsource-backed
Transcriptomic analysis identified 852 differentially expressed genes, with significant enriched pathways including hypoxia-inducible factor signaling, glycolysis/gluconeogenesis, and IL-17-mediated immunity.