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. 2018 Feb 21;8:3438. doi: 10.1038/s41598-018-21720-3

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© The Author(s) 2018

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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Malat1 gene expression in HUVECs and HK-2 cells is transcriptionally activated by HIF-1α (=HIF1a). Upstream promoter region of Malat1 spanning 5 kb from the transcriptional start site (TSS) identifies 1 putative Hypoxia Response Elements (HRE) and 2 HIF1 ancillary sequence in mice as well as 1 putative Hypoxia Response Elements (HRE) and 1 HIF1 ancillary sequence in humans (A). Transcriptional activation of HIF-1α in hypoxic HUVECs (B) and HK-2 cells (E) detected by transcriptional activation ELISA (n = 4). qPCR of Malat1 primer amplifying the HIF-1α– promoter region after immunoprecipitation of hypoxic HUVECs (C) and HK-2 cells (F) (n = 5). Malat1 expression after Dimethyloxaloylglycin (DMOG) treatment of HUVECs (D) and HK-2 cells (G) for 24 h. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001. ChIP = Chromatin immunoprecipitation, HIF-1α = Hypoxia-inducible factor 1 alpha, TSS = Transcriptional Start Site.