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3 In normoxia, HIF1A protein is targeted for degradation by cytosolic prolyl hydroxylases, while in hypoxia, these prolyl hydroxylases are inhibited, allowing HIF1A to translocate to the nucleus, dimerize with HIF1 protein, and the dimer then binds to hypoxia response elements to modulate transcription of target genes, prompting changes in metabolism and angiogenesis to promote survival

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The wt, gpoA, tpxD and ahpD mutants grew significantly more in nox2 -KO, which also present low ROS levels [22], than in the wt PLB-985 cells (Fig