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. 2022 Oct 20;36(11):2586–2595. doi: 10.1038/s41375-022-01696-w

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© The Author(s) 2022

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 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/.

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Fig. 7 — A The m⁶A abundances of ITGA4 mRNA transcripts in METTL3-overexpressing and control THP-1 cells as detected by m⁶A-seq (n = 3). Dotted boxes indicate regions for qPCR in (B). B Increasing m⁶A modification in specific regions of ITGA4 transcripts upon METTL3 overexpression as tested by gene-specific m⁶A-qPCR assays of THP-1 and Kasumi-1 cells. C Dual-luciferase reporter assays showing the effect of METTL3 and METTL3-CD on ITGA4 reporters with either wild-type or mutated m⁶A sites. *P < 0.05, **P < 0.01; t test. n ≥ 3, mean ± SD values are shown for (B) and (C).