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. 2018 Nov 30;8:17492. doi: 10.1038/s41598-018-35681-0

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© The Author(s) 2018

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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(a) Venn diagrams from IPA analysis of regulated proteins by ATRA at E10.5 and E11.5 in our study compared to proteins involved in neural crest process or linked to craniofacial development. Underlined, Fn1, Ybx1 and Parp1 are dysregulated in the same way at E10.5 and E11.5. In bold, Eftud2 and Gnai3 proteins were inhibited at E10.5. These genes are involved in craniofacial disorders: Mandibulofacial dysostosis (Guion-Almeida type) and Auriculocondylar syndrome 1 respectively. (b) Eftud2 and Gnai3 STRING network analysis. STRING network revealed protein related to Eftud2 and Gnai3 (highlighted in yellow) proteins based on literature references. Among proteins revealed by this software, some were also found dysregulated in our proteomics data. Thus, framed proteins were found increased (red), decreased (green) or differentially regulated (purple) following 1 and/or 2 days of ATRA treatment.