The Hypoxia Inducible Factors are a family of dimeric transcriptional regulators which play an important role in oxidative homeostasis during hypoxic conditions. HIF-1 is composed of alpha and beta subunits, represented by HIF-1 alpha and HIF-1 beta antibody products, both of which are well represented on our antibody database.
HIF-1 is an oxygen-sensitive complex, essential to hypoxic regulation during embryonic vascular development. In humans, the HIF-1 alpha subunit is encoded by the HIF1A gene, whereas the HIF-1 beta subunit is encoded by the ARNT (Aryl Hydrocarbon Receptor Nuclear Translocator) gene.
In normoxic conditions, the two subunits are dissociated. HIF-1 beta is located in the nucleus, and HIF-1 alpha in the cytoplasm, where it is rapidly degraded following HIF prolyl-hydroxylase activation. During hypoxia, HIF prolyl-hydroxylase is inhibited, leading to an increase in HIF-1 alpha levels. The alpha subunit then translocates to the nucleus, forming a stable HIF-1 dimer with the HIF-1 beta subunit.
Recent HIF-1 research has indicated HIF-1 stabilisation during hypoxia promotes mRNA stabilization and upregulation of a number of genes, including vascular endothelial growth factor (VEGF). This protein protects the growing embryo during periods of inadequate oxygen delivery, by promoting angiogenesis. However, the HIF-1 complex is also activated during solid tumour formation, owing to increased oxygen demand.
Currently, the HIF-1 beta antibody is one of the products being used to investigate induction of the HIF-1 complex in normoxic cells. It has been shown that chronic inflammatory conditions may cause aberrant functioning of transcription factors such as HIF-1, resulting in altered expression of chemokines, growth factor etc. This in turn may provide ideal “growing conditions” for metastasis and cancer.
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