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. 2019 Jan 24;9:747. doi: 10.1038/s41598-018-37342-8

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© The Author(s) 2019

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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Postulated mechanism for ceramide dependent regulation of G-CSF signaling in BMCs. In WT cells, G-CSF leads to the translocation and activation of G-CSF-R followed by the phosphorylation of Lyn kinase and of STAT3. This ultimately results in the expression of CXCR2 and its translocation into DRMs. Furthermore, G-CSF leads to downregulation of ceramides (CerS2 WT) and to upregulation of glycosylated very long chain ceramides in the plasma membrane. In CerS2 null cells, G-CSF did not induce the translocation of the G-CSF-R or the phosphorylation of Lyn, while the expression of CXCR2 was impaired. Moreover, due to the lack of CerS2, G-CSF induces upregulation of glycosylated long chain ceramides, leading to an altered lipid composition of the plasma membrane of CerS2 null cells in comparison to WT cells. In CerS6 null cells, G-CSF signaling and membrane composition is comparable to that in WT cells. The diagram of the displayed pathway was created using Biomedical-PPT-Toolkit-Suite (motifolio.com).