The hypoxia-inducible factor HIF drives transcription of the gene cyp-36A1, which encodes a cytochrome P450 enzyme that acts via a putative intercellular signal to regulate the nuclear receptor NHR-46 and consequently stress resistance and behavior.

Measurements of bar-headed geese flying in a wind tunnel in hypoxia reveal that these birds sustain aerobic flight at high altitude via a reduction in metabolism.

In mouse cardiomyocytes, (lymph)angiogenic growth factors are induced during early hypoxia by a translational mechanism involving a new IRES trans-acting factor, vasohibin-1.

Evolutionarily conserved hypoxic stress response genes are depleted for association with expression quantitative trait loci.

RNA profiles from lungs of mice exposed to intermittent hypoxia shared similarity with gene expression changes in human lung from patients with pulmonary diseases, including pulmonary hypertension, COPD, and asthma.

Under hypoxic stress, when cellular demand for energy relies entirely on glycolysis, the machinery for glycolysis binds RNA and phase separates into G bodies, leading to enhanced glycolysis rates.

Neural progenitors reside in relative low oxygen in the subgranular zone (SGZ), and the higher tissue oxygen levels that these cells must face as they migrate away from the hypoxic areas and differentiate appear to cause oxidative damage and an early phase of cell death.

Cellular stress in a disease-relevant cell type uncovers novel genetic effects on gene expression, which is likely relevant for disease.

Systemic hypoxia model reveals the detrimental effect of hypoxia on mitochondrial biogenesis in activated T-cells and points at a new approach for improving viral resistance in patients with respiratory diseases.

The subcellular localization of the prolyl hydroxylase oxygen sensor in C. elegans neurons is regulated by p38 MAP kinase signaling.