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. 2013 Mar;33(6):1149–1163. doi: 10.1128/MCB.06407-11

Fig 2.

Fig 2

TAK1 promotes BCL10 degradation independent of its kinase activity in lymphocytes. TAK1/ DT40 cells were retrovirally reconstituted with Flag-TAK1 or kinase-dead Flag-TAK1 (KD) and stimulated with 1 μg/ml ionomycin and increasing doses (3.9, 7.8, 31.2, and 250 nM) of PMA for 2 h (A) or 1 μg/ml ionomycin and 250 nM PMA for 0 to 20 min (B). WT and TAK1/ DT40 B cells (C) or EL4 T cells (D) were pretreated with the indicated doses of the TAK1 inhibitor 5Z-7-oxozeaenol followed by CHX and then stimulated with P/I (250 nM/1 μg/ml) for 0 to 180 min. Cells were lysed with RIPA buffer and immunoblotted as indicated to the left of each blot. The signal intensities of BCL10 levels relative to those of ERK were measured as described in Materials and Methods and are shown below the BCL10 immunoblots.