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. 2024 Jan 5;43(8):578–593. doi: 10.1038/s41388-023-02926-w

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© The Author(s) 2024

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. 1 — A Scheme for the disruption of the YAP-B-MYB interaction by MY-COMP. B HeLa cells were stably transfected with expression constructs for inducible MY-COMP or MY-COMP (2–79). Cell lines were treated with the indicated dose of doxycycline and the expression of MY-COMP was analyzed by immunoblotting with an anti-HA antibody. Actin served as a loading control. C HeLa cells were transfected with the indicated expression constructs. Flag-YAP was immunoprecipitated and bound HA-B-MYB was detected by immunoblotting. When MY-COMP was co-transfected, the interaction between flag-YAP and HA-B-MYB was decreased. Input: 3% of the lysate. D The expression of GFP or of the indicated MY-COMP constructs coupled to GFP through a T2A site was induced by doxycycline. FACS was performed to determine the percentage of in different phases of the cell cycle. GFP-positive cells (expressing MY-COMP) were analyzed. E Quantification of the results shown in D. Error bars indicate SDs. n = 3 independent replicates. Student’s t test. *p < 0.05, ns not significant.