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. Author manuscript; available in PMC: 2015 Jan 15.
Published in final edited form as: Biochem Pharmacol. 2013 Nov 22;87(2):332–343. doi: 10.1016/j.bcp.2013.11.006

Fig. 2.

Fig. 2

Inhibition of Erk1/2 blocks hsBAFF-enhanced cell proliferation and viability in B cells. Raji cells and purified mouse splenic B lymphocytes were treated with 0, 1, 2.5 μg/mL hsBAFF for 12 h (for Western blotting) or 48 h (for cell proliferation/viability assay) following pretreatment with/without U0126 (5 μM) or PD98059 (10 μM) for 1 h. Total cell lysates were subjected to Western blotting using indicated antibodies (A). The blots were probed for β-actin as a loading control. Similar results were observed in at least three independent experiments. The cell proliferation was evaluated by cell counting (B) and the cell viability was determined by the MTS assay (C). (A) hsBAFF-induced phosphorylation of Erk1/2 was severely blocked by U0126 or PD98059. (B and C) U0126 or PD98059 markedly inhibited hsBAFF-stimulated cell proliferation and cell viability, respectively. Results are presented as mean ± SE (n = 6). aP <0.05, bP <0.01, difference vs 0 μg/mL hsBAFF group; cp<0.01, difference vs 1 μg/mL hsBAFF group; dp<0.01, difference vs 2.5 μg/mL hsBAFF group.