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. 2023 Oct 17;42(46):3371–3384. doi: 10.1038/s41388-023-02859-4

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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. 4 — A The Notch (left), Wnt/β-catenin (middle), and Hh (right) pathway components modulated by p63 isoforms during ESCs’ stemness regulation. All the encircled numbers indicate p63 isoform contribution by transcription regulation. B The reciprocal miRNA-p63 interactions are a vital factor in modulating p63 function, which is extensively involved in the development of the skin epidermis, including epithelial cell proliferation, differentiation, and senescence. C p63 regulates the stemness of ESCs through the signal molecules associated with epigenetic modifications. D ΔNp63 controls the stemness of ESCs by regulating cell adhesion molecules. E Other signaling involved in p63-mediated modulation of ESCs’ stemness. As shown, ΔNp63 is the most studied isoform and it is involved in various cell mechanisms to achieve self-renewal and differentiation control of ESCs.