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. 2015 Apr 23;6(4):e1730. doi: 10.1038/cddis.2015.66

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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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p65^+/−-CM activates an HGF/Met/GSK3β pathway in RAW cells. (a) Western blot demonstrated that activation of RAW cells in PM induced an increase in pS9-GSK3β within 30 min (left), a response that was amplified by both WT- (middle) and p65^+/−-CM (right). (b) Densitometric analysis revealed that when activated in p65^+/−-CM, the fraction of pS9-GSK3β increased by 3.5-fold in 30 min, an amount significantly higher than WT-CM and PM groups (*P⩽0.05). (c) Inhibition of Met by SU11274 blocked pS9-GSK3β in RAW cells 30 min after exposure to LPS and p65^+/−-CM (d) in a dose-dependent manner (*versus SF+LPS, ⁺versus no LPS, P<0.05) Data are represented as mean±S.E.M. of at least three independent experiments