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. 2019 Aug 14;9:11861. doi: 10.1038/s41598-019-47891-1

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Molecular mechanism of ER-INP anti-PHD2’s promotion of angiogenesis via HIF-1α stabilization and transactivation under normoxia. ER-INP intrabody binds to PHD2 and blocks PHD2 hydroxylase activity to prevent the hydroxylation, ubiquitination, and degradation of HIF-1α. HIF-1α accumulation forms dimers by binding with HIF-1β and transactivates target genes at the consensus hypoxia-responsive elements 5′-(A/G) GGTG-3′. HIF-1α target genes control numerous key cellular processes, such as angiogenesis and metabolism. HIF-1α accumulation can promote MMP-13 expression, which can also promote angiogenesis.