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. 2015 Sep 17;6(9):e1890. doi: 10.1038/cddis.2015.232

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Copyright © 2015 Macmillan Publishers Limited

Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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C₂-ceramide-mediated SGK-1 expression is activated via p38/MAPK, cAMP/PKA and PI3K pathways. HEK-293 cells stably transfected with SGK-1wt were treated with C₂-ceramide (50 μM), C₂-Dihy (50 μM), SB202190 (10 μM) (p38 inhibitor), H-89 (10 μM) (PKA inhibitor) and LY294002 (30 μM) (PI3K inhibitor). After 48 h, SGK-1 expression was evaluated with antibodies specific for SGK-1. The protein levels of SGK-1 were compared with Tubulin levels. Results were confirmed in at least three separate experiments. Blots shown are representative of three independent experiments. Tubulin was used as a loading control (a). A quantification of three independent experiments by scanning densitometry is shown in (b) (*P<0.05, **P<0.01; N=3). The Ratio between C₂-ceramide (C2) and C2-Dihy or C₂-ceramide with inhibitors (C2/C2SB, C2/C2H89, C2/C2LY) was evaluated (c), *P<0.05, C2/C2-Dihy versus C2/C2SB, C2/C2H89; N=3. Results are expressed as means±S.D.