Supplementary Figure 1 from (+)-2-(1-Hydroxyl-4-Oxocyclohexyl) Ethyl Caffeate Suppresses Solar UV-Induced Skin Carcinogenesis by Targeting PI3K, ERK1/2, and p38

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PDF file - 139 KB, The p110alpha, ERK1, ERK2, and p38alpha protein kinases are major targets of HOEC. (A) HOEC inhibits p110alpha (a), ERK1 (b), ERK2 (c), and p38alpha (d) kinase activities. In vitro p110alpha, ERK1, ERK2, and p38alpha kinase assays were performed as described in Materials and Methods. Equal loading controls are shown as a Coomassie Blue (C.B) stained panel below each experiment. (B) HOEC directly binds with p110alpha, ERK1, ERK2, and p38alpha in vitro (a) and ex vivo (b). In vitro and ex vivo pull-down assays were perfomed using active kinases and solar UV-treated JB6 Cl41 cell lysates with sepharose 4B beads only or HOEC-conjugated sepharose 4B beads as described in Materials and Methods. Lane 1 shows input control and representative blots from 3 independent experiments are shown. Equal loading controls are shown as a Coomassie Blue (C.B) stained panel below each experiment. (C) HOEC competitively binds with ATP to p110alpha, ERK1, ERK2, and p38alpha. In vitro ATP competitive pull-down assays were perfomed using active kinases with HOEC-conjugated-sepharose 4B or sepharose 4B beads only as described in Materials and Methods. The pulled down proteins were detected by Western blot analysis. All input controls were used as a standard for each protein in the first lane of the pull-down assay results. The relative abundance of each band normalized to its own control group (untreated, set at 1) was quantified and the value is shown above each respective lane in each blot.

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