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. 2022 Nov 9;13:6762. doi: 10.1038/s41467-022-34434-y

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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 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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Fig. 7 — a Venn diagram showing the comparison of differentially methylated transcripts and differentially expressed transcripts identified in the exercise-induced cardiac hypertrophy murine model. DMG, differentially m⁶A methylated genes. DEG, differentially expressed genes. b KEGG analysis of significantly enriched m⁶A methylated peaks (p < 0.05; fold-change > 2.0) in control group and swim group, respectively. c Representative western blot and statistical data of phosphorylation levels of Akt-S473, Akt-T308 in NRCMs with or without METTL14 knockdown (n = 6 wells/group). d The methylation levels of Phlpp2 mRNA in swim and control mouse hearts measured by MazF-qPCR (n = 6 mice/group). The levels of a targeted amplicon (labeled “T”) is measured against a control (labeled “C”) amplicon in a MazF-digested sample and normalized against a nondigested sample. e Western blot analyses of PHLPP2 in whole lysates isolated from swim and control murine hearts (n = 6 mice/group). f Western blot analyses of PHLPP2 and METTL14 in NRCM with or without METTL14 inhibition (n = 6 wells/group). g m⁶A enrichment levels in Phlpp2 mRNA in H9C2 cardiomyocytes treated as indicated using m⁶A-RIP (meRIP)-qPCR (n = 5/group). h Relative luciferase activity of Rattus PHLPP2 wild-type (PHLPP2-WT-pGL3) or m⁶A mutant (PHLPP2-mut-pGL3) reporter gene with or without Rattus METTL14 overexpression (n = 6/group). i Relative luciferase activity of Rattus PHLPP2-WT-pGL3 reporter gene with Rattus wild-type METTL14 (WT^METTL14) or mutant METTL14 (R234/235A-R278P-D292A^METTL14) overexpression (n = 6/group). j Representative western blot and statistical data of PHLPP2 and phosphorylation level of Akt-S473 in NRCMs with WT^METTL14 or R234/235A-R278P-D292A^METTL14 overexpression (n = 6/group). k MazF-qPCR identified the methylation modification region of Phlpp2 mRNA which is specifically regulated by METTL14 (n = 6/group). The levels of a targeted amplicon (labeled “T”) is measured against a control (labeled “C”) amplicon in a MazF-digested sample and normalized against a nondigested sample. NRCM, neonatal rat cardiomyocyte; shScr, Scramble short hairpin RNA; shMETTL14, METTL14 short hairpin RNA to knockdown METTL14. ns, nonstatistically significant. All data are expressed as means ± SD. c–f, k Independent-sample t-test, two-sided; g two-way ANOVA followed by Tukey’s post hoc test; h, j one-way ANOVA followed by Bonferroni test; i one-way ANOVA followed by Dunnett T3 test.) Source data are provided as a Source Data file.