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. 2014 Aug 4;11:135. doi: 10.1186/1742-2094-11-135

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Copyright © 2014 Liu et al.; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. 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.

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TSG-6 suppresses LPS-mediated phosphorylation of p38, JNK, and Erk. BV2 cells were stimulated with LPS in the presence and absence of rmTSG-6 (10 ng/ml) for the indicated times. Cell lysates were analyzed for the phosphorylated levels of p38, JNK, Erk, and their total levels by western blotting with the respective specific antibodies. (A) Representative image of protein levels of P38, JNK, and Erk. (B-D) The phospho:total ratios of p38 (B), JNK (C), and Erk (D) were determined by measurements of band intensities of each protein kinase and quantified as fold changes over the control (unstimulated BV2 cells). X axis are shown in time slots of 15, 30, and 60 minutes. Values are mean ± SD. n = 3; **P <0.01; significantly different from LPS-treated cells. Abbreviations: LPS, lipopolysaccharide.