Hypoxia-Inducible Factor (HIF) is a transcriptional regulator that plays a central role in controlling the cellular response to low oxygen conditions (hypoxia). Comprising a family of heterodimeric transcription factors, HIFs are key players in adapting cells to hypoxic environments, regulating the expression of a wide range of genes involved in oxygen homeostasis, energy metabolism, angiogenesis, and other processes critical for cell survival and adaptation.The HIF family consists of α and β subunits, with the α subunit being the primary regulatory component that responds to oxygen levels. There are three main isoforms of the HIF-α subunit: HIF-1α, HIF-2α, and HIF-3α. HIF-β, also known as ARNT (Aryl Hydrocarbon Receptor Nuclear Translocator), forms a heterodimer with the α subunit to facilitate its transcriptional activity. Under normoxic conditions (normal oxygen levels), HIF-α subunits are hydroxylated by a group of enzymes called prolyl hydroxylases (PHDs) at specific proline residues. This hydroxylation marks HIF-α for recognition by the von Hippel-Lindau (VHL) protein, which is part of an E3 ubiquitin ligase complex. The VHL-mediated ubiquitination leads to the degradation of HIF-α via the proteasome under normal oxygen conditions. In hypoxic conditions, oxygen-dependent prolyl hydroxylation of HIF-α is impaired due to the limited availability of oxygen. As a result, HIF-α subunits escape degradation and accumulate in the cytoplasm. This accumulation permits their translocation to the nucleus, where they heterodimerize with HIF-β/ARNT to form the active transcription factor complex. In the nucleus the HIF complex binds to specific DNA sequences known as hypoxia response elements (HREs) within the promoter regions of target genes. This leads to the recruitment of coactivators and initiation of transcription, resulting in the upregulation of genes involved in various adaptive responses to hypoxia. HIF regulates a diverse set of genes that collectively mediate the cellular response to hypoxia. HIF stimulates the expression of genes involved in angiogenesis, such as vascular endothelial growth factor (VEGF), to promote the formation of new blood vessels and enhance oxygen delivery to tissues. HIF also upregulates glycolytic enzymes and glucose transporters, acting to shift cellular metabolism towards anaerobic glycolysis for ATP production in oxygen-depleted conditions. HIF also induces the expression of erythropoietin (EPO), a hormone produced by the kidney that stimulates red blood cell production in bone marrow to increase oxygen-carrying capacity of the body. Concurrently, HIF also controls genes involved in iron metabolism and transport, adapting cells to low oxygen by modulating iron availability. Finally, HIF promotes the expression of anti-apoptotic factors and regulators of cell survival to counteract hypoxia-induced cell death.Thus, by influencing the expression of a wide array of target genes, HIF enables cells to adapt and survive under low oxygen environments, making it a central player in both normal physiological responses and pathological adaptations to hypoxia-related disorders. We provide a comprehensive product range of research tools for studying HIF, including HIF-1 alpha antibodies, HIF1 beta antibodies, and HIF-1 alpha ELISA Kits. Explore our full HIF product range below and discover more, for less.