HIF-2 alpha Recombinant Rabbit mAb (S-5326)

HIF-2α (hypoxia-inducible factor 2α), also known as EPAS1, is a basic helix-loop-helix transcription factor encoded by the EPAS1 gene and is a core member of the HIF family. It shares high homology with HIF-1α but possesses distinct spatiotemporal expression patterns and target gene preferences, being stably expressed primarily in specific cell types such as vascular endothelial cells, renal interstitial cells, hepatic parenchymal cells, and neural crest cells. Under normoxic conditions, proline residues of HIF-2α are hydroxylated by PHDs and recognized by the VHL protein, leading to degradation via the ubiquitin-proteasome pathway; under hypoxia, however, its degradation is blocked, allowing it to translocate to the nucleus and form a heterodimer with ARNT (HIF-1β) to activate the transcription of a series of target genes. HIF-2α is particularly adept at regulating genes such as erythropoietin (EPO), VEGF, TGF-α, and Oct-4, thereby profoundly influencing erythropoiesis, vascular remodeling, lipid metabolism, embryonic development, and the maintenance of cancer stem cells. It is highly expressed in various cancers including renal cell carcinoma, pheochromocytoma, and hepatocellular carcinoma, and is frequently associated with tumor aggressiveness, therapeutic resistance, and poor prognosis, while also participating in the pathological processes of pulmonary hypertension and chronic kidney disease. Notably, although HIF-2α and HIF-1α coordinately respond to hypoxia, they exhibit distinct division of labor in terms of target gene selectivity, activation kinetics, and physiological roles—for example, HIF-2α plays a more dominant role in long-term adaptive hypoxic responses.