ZHX2 controls HIF1α oncogenic signaling and tumorigenesis in triple-negative breast cancer.

The prolyl hydroxylase domain 2 regulates the Treg development and function in a hypoxia-inducible factor 2α-dependent manner.

KSHV nullifies hypoxic restriction of DNA replication.

Oxygen-independent (pseudohypoxic) HIF pathway activation is a core determinant of dysregulated collagen-structure function in human fibrosis.

The current findings address the redox regulation of hypoxia inducible factor 1α (HIF1α) stability in hypoxia by showing that cytosolic, mitochondrial or lipid ROS are not necessary for HIF1α stabilization in hypoxia.

An unbiased genome-wide human forward genetic screen identifies the vacuolar ATPase complex and assembly factors as regulators of HIF stability through their actions on intracellular iron metabolism.

Previous studies and emerging data on pseudohypoxic diseases suggest that the complex phenotypic spectrum of VHL disease is due to the extent of HIF pathway deregulation in susceptible cell types and not by other purported substrates or functions of pVHL.

During pathogen infection, natural killer cells require hypoxia-inducible factor-1α for optimal metabolism to prevent apoptosis, thereby reducing viral load and protecting against morbidity.

Radiotelemetric and genetic studies of peripheral tissue response show that a peripheral tissue can dynamically alter cardiovascular adaptation to changes in environmental oxygen.

A survey of oxygen-dependent enzymes suggests new candidates for oxygen sensors, expanding potential mechanisms underlying hypoxia-related adaptations or diseases in humans.