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. 2009 Sep;11(9):846–855. doi: 10.1593/neo.09528

Figure 1.

Figure 1

IL-12 deficiency enhances photocarcinogenesis in mice and enhances activation of the cell survival kinases, PI3K, Akt, and MAPK in long-term UV-exposed mouse skin. (A and B) IL-12-deficient mice have a greater number of tumors per group and larger tumor volume/tumor than WT mice, n = 20. Significant difference versus WT mice, *P < .001. (C) The expression levels of PI3Kp85 (regulatory) and PI3Kp110 (catalytic) and the phosphorylation of Akt (Ser473) are enhanced in UV-exposed skin, and there is greater enhancement in the UVB-exposed IL-12-deficient mouse skin than in the UVB-exposed WT mouse skin. (D) The phosphorylation of ERK1/2 and p38 proteins is enhanced in long-term UV-exposed skin, and this effect is more pronounced in the UVB-exposed IL-12-deficient mouse skin than in the UVB-exposed WT mouse skin. Data were compared with those obtained using skin samples from age-matched non-UVB-exposed control mice. Representative blots are shown from three independent experiments in which almost identical results were observed.