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. 2018 Oct 19;8:15467. doi: 10.1038/s41598-018-33769-1

Figure 4.

Figure 4

SHIP1-deficiency compensates for signalling defects in BTK-deficient BMMCs. (a) WT, Btk−/−, Ship1−/−, and DKO BMMCs or (b) WT and Ship1−/− BMMCs, pre-treated with 0.3 µM Ibrutinib or vehicle (DMSO) for 30 min, were left untreated (con) or stimulated with suboptimal and optimal concentrations of Ag (DNP-HSA [DNP]) for 1 and 5 minutes. Whole-cell lysates were subjected to Western Blot analysis with the indicated antibodies against P-IKKα/β (Ser176/Ser177), P-PKB (Ser473), P-ERK1/2 (Thr202/Tyr204), P-p38 (Thr180/Tyr182), P-IκBα (Ser32), and p85 (loading control). Comparable results were obtained in at least three experiments with different BMMC cultures. Fine vertical lines were inserted to allow for better discrimination of cells/conditions. Because proteins of comparable size were analysed, the same lysates were separated on two gels with an anti-p85 loading control on each gel (a; marked with/without asterisk).