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. 2009 Oct 7;106(43):18279–18284. doi: 10.1073/pnas.0906328106

Fig. 3.

Fig. 3.

Miz1 does not inhibit JNK1 activation by IL-1β and UV or activation of ERK, p38, and IKK by TNF-α. (A and B) WT fibroblasts were transfected with the control scramble siRNA or siRNA of Miz1 (siMiz1) (100 nM of each). Expression of Miz1, phosphorylation and expression of JNK and c-Jun, and JNK activity in response to IL-1β (2 ng/mL, 15 min) (A) or UV (20 J/m2, 30 min) (B) were analyzed by immunoblotting and immune complex kinase assays, respectively. (C) The effect of Miz1 silencing on TNF-α-induced activation of ERK and p38 was determined as described in A and B. (D–F) Effects of the loss of Miz1 on TNF-α-induced IKK phosphorylation (D) and activation (IκBα degradation) were analyzed by immunoblotting using corresponding antibodies. The effect of the loss of Miz1 on TNF-α-induced NF-κB activation was measured by a NF-κB reporter gene assay, as described (13) (F).