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. 2022 Jul 7;20:102. doi: 10.1186/s12964-022-00911-6

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© The Author(s) 2022

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 7 — Dominant roles of PI3Kβ in EGF-induced CDR formation. A Representative confocal images of actin in Hep3B with or without p110α inhibitor (A66) or/and p110β inhibitor (TGX221) treatment after EGF stimulation. Arrows indicate CDRs. (B Quantification of the frequency of CDRs after stimulation by EGF with/without p110 inhibitors from three independent experiments. TGX221 completely blocked CDR. *P < 0.05, ****P < 0.0001, by one-way ANOVA. C A66 completely blocked EGF-stimulated (5 min) pAKT. TGX211 attenuated pAKT around 50%. D Quantification of pAKT/AKT ratios after EGF stimulation (5 min) with/without p110 inhibitors from 3 independent experiments. Results are indicated as arbitrary units (AU). ***P < 0.001, ****P < 0.0001, by one-way ANOVA