HIF-2-alpha overexpression 293T lysate (whole cell)

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

HIF-2-alpha also known as hypoxia-inducible factor 2-alpha or EPAS1 plays a significant role in cellular response to oxygen levels. Mechanically HIF-2-alpha functions as a transcription factor that activates certain genes when oxygen is low. The protein typically weighs around 118 kDa. It is expressed in various tissues but particularly in endothelial cells and some neuronal tissues. These sites highlight its importance in organs requiring tight regulation of oxygen.

Biological function summary

HIF-2-alpha regulates the expression of genes involved in energy metabolism and angiogenesis. The protein forms a complex by dimerizing with the HIF-1-beta subunit which is necessary for transcriptional activity. Through this complex formation and activity it influences processes such as erythropoiesis and regulates factors like vascular endothelial growth factor (VEGF). Therefore HIF-2-alpha contributes to the adaptation of cells and tissues under hypoxic conditions.

Pathways

HIF-2-alpha engages in the hypoxia signaling pathway playing an essential part by modulating gene expression in response to low oxygen availability. This role impacts other proteins such as HIF-1-alpha sharing overlapping functions but with distinct target genes. Additionally HIF-2-alpha is involved in the mTOR pathway which influences cell growth and metabolism through its interaction with the nutrient-sensing regulatory pathway.

Researchers have linked HIF-2-alpha with conditions like renal cell carcinoma and pulmonary hypertension. The protein's dysregulation can lead to altered expression of angiogenic factors promoting tumor growth and survival. In particular its connection with VEGF exemplifies its role in these pathologies by facilitating aberrant blood vessel formation. Such interactions further highlight the potential of HIF-2-alpha as a therapeutic target in disease modulation.