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. 2023 Mar 2;51(9):4284–4301. doi: 10.1093/nar/gkad120

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© The Author(s) 2023. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Figure 8. — G9a and YAP are crucial for BACH1-induced repression of VSMC marker genes. (A) Immunoblotting showed that BACH1-induced decreases of ACTA2 and CNN1 protein were abolished by the G9a inhibitor BIX-01294 (n = 4 independent experiments, data are mean ± SD. One-way ANOVA followed by Tukey post-hoc tests). (B) Immunoblotting showed that BACH1-induced decreases of ACTA2 and CNN1 protein were abolished by silencing of G9a. Quantitative and statistical analysis are shown in Online Figure VIB. (n = 4 independent experiments, data are mean ± SD. One-way ANOVA followed by Tukey post-hoc tests). (C) Immunoblotting showed that BACH1-induced decreases of ACTA2 and CNN1 protein were abolished by silencing of YAP. Quantitative and statistical analysis are shown in Online Figure VIB (n = 3 independent experiments, data are mean ± SD. One-way ANOVA followed by Tukey post-hoc tests). (D) Schematic review showed that BACH1 suppresses the VSMC contractile phenotype and regulates the chromatin accessibility by the recruitment of G9a and YAP and maintains the H3K9me2 state on VSMC marker genes’ promoters.