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. 2023 Jan 11;6:29. doi: 10.1038/s42003-023-04416-x

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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. 9 — a ZNF185 is localized to the perinuclear region under basal conditions in endothelial cells. N-terminal region of ZNF185 interacts with actin. b C-terminal region of ZNF185 interacts with PKA, which phosphorylates ZNF185. Both phospho-ZNF185 and F-actin accumulate at the membrane region in response to forskolin and stabilize cortical actin structures. c ZNF185 knockdown activates RhoA and promotes actin stress fiber formation, causing endothelial hyperpermeability. ZNF185 is essential for cAMP/PKA-induced RhoA inhibition. d The thrombin protease divides ZNF185 into an N-terminal actin-targeting domain and a C-terminal PKA-interacting domain, which may cause RhoA activation and stress fiber formation. Schematics were created with BioRender.com.