Skip to main content
. Author manuscript; available in PMC: 2011 Jan 15.
Published in final edited form as: Cancer Res. 2010 Jul 7;70(14):5797–5806. doi: 10.1158/0008-5472.CAN-09-3669

Figure 4.

Figure 4

MKK4 is required for mediating the phosphorylation of JNK in the epidermis of the skins treated with DMBA/TPA. mkk4skin+/+ and mkk4skin−/− animals were treated with DMBA/TPA. Controls correspond to age matched untreated mkk4skin+/+ mice. Skin biopsies and tumors were isolated 20 weeks later. Sections were immunostained with the antibodies indicated. Immunostaining with a specific antibody to MKK4 confirms the loss of MKK4 in the epidermis of mkk4fl/fl mice expressing the K14-CreERT2 transgene and treated with tamoxifen. The absence of MKK4 prevents increased JNK2 expression following DMBA/TPA treatment. In contrast, the level of JNK1 is reduced in the wild type skin treated with DMBA/TPA. Immunostaining with a specific antibody to phospho (P)-JNK demonstrates that DMBA/TPA induces the phosphorylation of JNK and that this is prevented by the loss of MKK4. Unless indicated otherwise, the pictures were taken at x63 magnification. Scale bar represents 20 μM.