Genes regulated by hypoxia play roles in mediating responses to low oxygen conditions. At the centre of the hypoxic response is hypoxia-inducible factor (HIF), a transcription factor composed of two subunits: an oxygen-sensitive α-subunit (HIF-α) and a constitutively expressed β-subunit (HIF-β or ARNT). In normoxic conditions, HIF-α undergoes hydroxylation by prolyl hydroxylases (PHDs), leading to its proteasomal degradation. Under hypoxic conditions, reduced oxygen availability inhibits PHD activity, allowing HIF-α to accumulate and form a heterodimer with HIF-β. HIF then translocates to the nucleus, binds to hypoxia response elements (HREs) within the promoters of target genes, initiating their transcription. HIF regulates the expression of these genes to ensure cellular adaptation, survival, and tissue homeostasis in oxygen-deprived environments. The functions of these genes are diverse, each contributing to the overall hypoxic response. A critical function of hypoxia-regulated genes is the promotion of angiogenesis. Genes such as vascular endothelial growth factor (VEGF) and angiopoietins are upregulated by HIF, stimulating the growth, and sprouting of new blood vessels. This process helps increase oxygen and nutrient delivery to tissues, improving their overall oxygen supply. HIF-induced genes also alter cellular metabolism towards glycolysis, the anaerobic breakdown of glucose. Glycolysis is favoured by the induction of genes encoding glucose transporters (GLUTs) and glycolytic enzymes such as hexokinase (HK) and pyruvate kinase (PK). In addition, HIF-1 induces the expression of lactate dehydrogenase A (LDHA), which catalyses the conversion of pyruvate to lactate. This metabolic shift sustains modest ATP production under oxygen-limiting conditions. Although less efficient, glycolysis provides a rapid means of generating ATP and supports cell survival when oxygen availability is compromised. Hypoxia-regulated genes also influence erythropoiesis, the production of red blood cells. Erythropoietin (EPO), a hormone that stimulates red blood cell production in bone marrow, is controlled by HIF. Under hypoxia, HIF induces EPO expression in the kidney, resulting in the generation of more red blood cells. This adaptive response increases the oxygen-carrying capacity of the blood, enhancing tissue oxygenation. Genes involved in iron homeostasis are also under the control of HIF. HIF regulates the expression of proteins such as transferrin and transferrin receptor (TfR) to optimize iron uptake and transport. This is important since iron is essential for multiple cellular processes, including oxygen transport and utilization. HIF-regulated genes also contribute to cell survival and protect cells from hypoxia-induced cell death (apoptosis). HIF promotes the expression of anti-apoptotic factors and regulators of cell survival pathways, helping cells survive low oxygen conditions. Finally, in addition to their physiological roles, hypoxia-regulated genes can contribute to disease progression. In cancer, for instance, the hypoxic microenvironment within solid tumours drives the expression of genes that promote survival, angiogenesis, and metastasis of cancer cells. HIFs also enhance the expression of genes encoding enzymes involved in the catabolism of extracellular matrix components, allowing tumour cells to also invade surrounding tissues, whilst HIF-mediated metabolic adaptations support the energy demands of rapidly dividing cancer cells. We provide a wide product range of research reagents for studying hypoxia regulated, including CD73 antibodies, Carbonic Anhydrase IX antibodies, ADFP antibodies, HIF-1 alpha ELISA Kits, and Visfatin ELISA Kits. Explore our full hypoxia regulated product range below and discover more, for less. Alternatively, you can explore our Hypoxia Regulated product range.