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. 2020 Oct 6;44(6):2364–2372. doi: 10.3892/or.2020.7792

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Copyright: © Zheng et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 1. — Upregulated AspH activates the Notch signaling pathway. HIF-1α controls AspH expression at the transcriptional level by interacting with the HRE. AspH upregulation promotes the release of the NICD from the Notch receptor. NICD enters the nucleus and forms a Notch transcription activation complex with RBPJ and MAML. Subsequently, the downstream Notch-responsive genes are activated. AspH, aspartate β-hydroxylase; NICD, Notch intracellular domain; NECD, Notch extracellular domain; HRE, hypoxia response element; HIF-1α, hypoxia-inducible factor 1α; MAML, mastermind-like; ADAM, a disintegrin and metalloproteinase; HES1, hairy and enhancer of split-1; HEY1, hairy-related transcription factor-1; EpCAM, epithelial cell adhesion molecule; PCNA, proliferating cell nuclear antigen; JAG, Jagged; RBJP, recombination signal binding protein Jκ; ADAM, a disintegrin and metalloproteinase.