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Effect of deletion of SphK1 on signaling pathways involved in GalN/LPS-induced acute liver failure. A and B, WT, SphK1−/−, and SphK2−/− mice were treated without or with GalN/LPS. n = 2-3 mice per group. One hour later, proteins in liver lysates were separated by SDS-PAGE and analyzed by immunoblotting with the indicated antibodies. Tubulin and GAPDH were used as loading controls
