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. 2020 May 9;27:62. doi: 10.1186/s12929-020-00655-w

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 6 — Notch pathway inhibitor DAPT rescues defective angiogenesis caused by knockdown of METTL3. a qRT-PCR and (b) western blot analysis of expression of target genes in control and METTL3 deficient endothelial cells which were treated with DMSO or DAPT, respectively. c Tube formation and (g) migration assay of control and METTL3 depletion cells after DMSO or DAPT treatment, respectively. Data are shown as mean ± SEM of three independent experiments. P values were calculated using two-way ANOVA followed by Student’s t-test. M, METTL3; D, DAPT; M × D, METTL3 × DAPT. *, P < 0.05; **, P < 0.01; ***, P < 0.001