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. Author manuscript; available in PMC: 2019 Jan 28.
Published in final edited form as: Annu Rev Pharmacol Toxicol. 2019 Jan 6;59:537–554. doi: 10.1146/annurev-pharmtox-010818-021031

Figure 2.

Figure 2

Model illustrating NiCl2 displacing Fe in prolyl hydroxylase domain. By displacing Fe in the PHD, Ni is able to inhibit HIF-prolyl- and asparaginyl-hydroxylases and promote the stabilization of HIFα proteins and HIF-1-dependent transcription. Abbreviations: Cl, chlorine; Fe, iron; HIF −1α, hypoxia-inducible factor 1α; His, histidine; IKKβ, nuclear factor kappa-B kinase subunit β inhibitor; M-MITF, microphthalmia-associated transcription factor type M; Ni, nickel; PHD, prolyl hydroxylase domain protein; TCA, tricarboxylic acid; TET, ten-eleven translocation; VEGF, vascular endothelial growth factor.