HIF-1a binding in wildtype and JAK2V617F mice in hypoxia and normoxia
Hypoxia-inducible factors (HIFs) are master transcriptional regulators, central to cellular survival under limited oxygen (hypoxia) and frequently activated within malignancy. Malignant context affects the role of HIFs within oncogenesis; however the mechanisms that regulate these context-disparities are not well understood. We therefore sought to determine whether HIF-1 function is determined by modality of activation, applying the JAK2V617F (JVF) model of myeloproliferative neoplasms (MPNs), in which HIF-1 is active in normal oxygen conditions (normoxia)