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. 2023 Aug 2;43(8):426–449. doi: 10.1080/10985549.2023.2229225

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© 2023 The Author(s). Published with license by Taylor & Francis Group, LLC.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way. The terms on which this article has been published allow the posting of the Accepted Manuscript in a repository by the author(s) or with their consent.

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FIG 1 — ATF3 is a p53 target gene that is activated via the ISR in a p53-independent manner. Western blot analysis of (A) ATF3 and (B) p53 with GAPDH as a loading control in HCT116 p53 WT (left) and p53 null cells (right) following a 6 h treatment with DMSO, 5 μM Nutlin-3A (NUT), 100 μM etoposide (ETOP), 2 μM tunicamycin (TM) or 2 mM histidinol (HisOH). Gene expression analysis of the (C) ATF3 gene (D) CDKN1A gene and (E) ASNS gene in HCT116 p53 WT (black) and HCT116 p53 null (pink) cells in response to 6 h treatment with stimuli. All statistical comparisons were computed using a one-way ANOVA test. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.