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. 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 5.

Figure 5

The loss of MKK4 prevents the phosphorylation of c-Jun in the skin treated with DMBA/TPA. mkk4skin+/+ and mkk4skin−/− animals were treated with DMBA/TPA. Controls correspond to age matched untreated mkk4skin+/+ mice. Sections of skin biopsies and tumors 20 weeks after TPA treatment were immunostained with antibodies to c-Jun, phospho (P)-c-Jun at Ser 73, EGFR, and p53. The results show that MKK4 is required for increased expression and phosphorylation of c-Jun, and increased expression of the c-Jun target EGFR. Elevated expression of p53 in MKK4-deficient epidermis of animals treated with DMBA/TPA is consistent with evidence that p53 is a tumor suppressor whose transcription can be repressed by c-Jun. Scale bar represents 20 μM.