Genome-wide mapping of HIF-2a binding under normoxia in human bronchial epithelial cells (BEAS-2B)

Growing number of cancer (stem) cells and stem cells were described to accommodate constituent active HIF-2a under normoxia. Previous study of hypoxia effect may have obscured some of normoxic HIF-2a functions as hypoxia inducible features. Our interest in study of protective potential of HIFs in lung cells led us to discover pseudohypoxia functions of HIF-2a under normoxia in human bronchial epithelial cells which exhibit pluripotency related markers and features. Our study provided perspective to pseudohypoxia functions of HIF-2a via enrichment of de novo motifs. In addition to the C-TAD, the N-TAD of HIF-2a was found to contribute to targeting on these non-canonical loci. Further elucidation of pseudohypoxia mechanism could resolve its implication of malignancy or pluripotency. Overall design: We report globally mapped binding of HIF-2a under normoxia by using high throughput sequencing