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. 2023 Dec 1;14(12):787. doi: 10.1038/s41419-023-06319-5

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© The Author(s) 2023

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. 5 — A Acetylated p53 at lysine 120 (aK120 p53) in Control or HDAC4 and 5 overexpressing C2C12 myoblasts also expressing wild type (WT), K120R (loss-of-function) or K120Q (gain-of-function) p53. B Expression of caspase 3 (Casp3; One-way ANOVA p = 0.0040 ×² = 0.8408), caspase 9 (Casp9; One-way ANOVA p = 0.0025 ×² = 0.8650), cytochrome c (Cycs; One-way ANOVA p = 0.0033 ×² = 0.8518) and the cystine/glutamate antiporter xCT (Slc7a11; One-way ANOVA p < 0.0001 ×² = 0.9769) in Control or HDAC4 and 5 overexpressing C2C12 myoblasts also expressing WT or K120Q p53 (Tukey’s multiple comparisons shown). C Percentage of apoptotic cells following exposure to camptothecin in Control or HDAC4 and 5 overexpressing C2C12 myoblasts also expressing WT or K120Q p53 (One-way ANOVA p = 0.0014 ×² = 0.8875, Tukey’s multiple comparisons shown). D Cell viability 16 h after palmitate exposure in C2C12 myoblasts expressing WT or K120Q p53 (Two-way ANOVA, treatment p < 0.0001 F(1,12) = 50.44, genotype p = 0.0361 F(1,12) = 5.56, significant Tukey’s multiple comparisons shown). E Cell viability in C2C12 myoblasts following palmitate exposure and co-incubation with vehicle (DMSO) or increasing concentrations of Z-DEVD-FMK (One-way ANOVA, p = 0.3282). F Schematic showing key regulatory points in the ferroptosis pathway. G Cell viability in C2C12 myoblasts following palmitate exposure and co-incubation with vehicle (DMSO) or increasing concentrations of Ferrostatin (One-way ANOVA, p = 0.0323 ×² = 0.5337, significant Tukey’s multiple comparisons shown). H Cell viability in Control or HDAC4 and 5 overexpressing C2C12 myoblasts following exposure to increasing concentrations of Erastin (Two-way ANOVA, genotype p < 0.0001 F(1,18) = 293.7, treatment p < 0.0001 F(2,18) = 139.6, interaction p < 0.0001 F(2,18) = 50.88, significant Tukey’s multiple comparisons shown). I Glutamate (Glu), glutathione (GSH) and the GSH/Glu ratio in Control or HDAC4 and 5 overexpressing C2C12 myoblasts (Unpaired t-tests). J Glutathione peroxidase (GPX) activity in Control or HDAC4 and 5 overexpressing C2C12 myoblasts (Unpaired t-test). K H₂O₂ derived from mitochondria (mito), NADPH oxidases (NOX) and other sources in Control or HDAC4 and 5 overexpressing C2C12 myoblasts (Unpaired t-tests). Data are mean ± SEM, n = 4–10 biological replicates per group.