Abstract
1 min read44kD; Erk2, 42 kD), p38/MAPK (38 kD) and the corresponding phosphorylated forms with specific antibodies. Equal protein loading was controlled by Ponceau S staining. The graph shows the mean values of the fold induction of the signals from the unphosphorylated and phosphorylated forms of Jnk, Erk, and p38/MAPK compared with the signals in control cells. Mean values and SDs were calculated from at least five independent experiments. SDs are shown by error bars. *, P < 0.05; **, P < 0.001, calculated by the two-tailed Student's test. (B) After CD40 triggering, LMP1/CD40-expressing cells are damped in activation compared with control cells. Splenic B cells of LMP1/CD40 and control mice were stimulated with α-CD40 antibody for the indicated time points, and Western blots were performed as described in A. Equal protein loading was controlled by tubulin staining. One representative experiment out of three is shown. (C) The improved survival of LMP1/CD40-expressing B cells is dependent on continuous Erk phosphorylation. Splenic B cells of LMP1/CD40 and control mice (CD19-Cre) were cultured for up to 5 d with the Mek1/2 inhibitor U0126 (dotted line) and the Jnk-inhibitor SP600125 (dashed line; triangle and square, respectively). As control, B cells from LMP1/CD40 and control mice were cultured in the presence of DMSO (continuous lines, rectangle, and circle, respectively). Percentages of living cells (Topro negative) were determined by flow cytometry at day 1, 3, and 5. The bars show mean percentages of living cells of three independent experiments. Error bars show the SD.<b>Copyright information:</b>Taken from "Constitutive CD40 signaling in B cells selectively activates the noncanonical NF-κB pathway and promotes lymphomagenesis"The Journal of Experimental Medicine 2008;205(6):1317-1329.Published online 9 Jun 2008PMCID:PMC2413030.
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