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. 2020 May 19;10:8285. doi: 10.1038/s41598-020-64873-w

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© The Author(s) 2020

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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The effects of Mettl4 knockdown on glucose metabolism. (a) Promoter 6 mA abundance of Insr gene on day(+2) of the differentiation was determined by 6mA-IP-qPCR. (b) Expressional profiles of Insr in wild-type and Mettl4 knockdown cells. Gene expression levels were determined by quantitative RT-qPCR, in relative to that of β-actin. (c) Knockdown of Mettl4 led to decreased consumption of glucose. (d) Fluorescence images of 2-NBDG uptake. (e) Quantitative analyses of 2-NBDG uptake. Data are analyzed by Student’s t-test and presented as mean ± s.d., n = 3 independent experiments. *P < 0.05; **P < 0.01.