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. 2020 Nov 19;10(4):2045894020913475. doi: 10.1177/2045894020913475

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© The Author(s) 2020

Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Fig. 3. — The hypoxia signaling pathway involves EGLN1-mediated hydroxylation and VHL-dependent ubiquitination of HIF-1α/2α subunits leading to its proteosomal degrardation under normoxic conditions. However, under hypobaric hypoxic conditions, HIF-1α/2α subunits are stabilized, which complexes with HIF-β subunit and drives transcriptional regulation of numerous genes involved in vascular homeostasis.

HIF: hypoxia-inducible factor; HRE: hypoxia response element; VHL: Von Hippel-Lindau; Ub: ubiquitin; indel: insertion–deletion; 3.4kb TED: Tibetan-enriched 3.4kb deletion; D4E: aspartate4glutamate; C127S: cysteine127serine; IKZF1: IKAROS family zinc finger 1; SP1: specificity protein 1; AP1: activator protein 1; EGLN1: Egl nine homolog 1; HAPE: high-altitude pulmonary edema; TF: transcription factor.

Note: Hash (#) represents high-altitude adaptation/maladaptation associated genetic variants.