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. 2012 Jul 31;7(7):e42271. doi: 10.1371/journal.pone.0042271

Figure 6. Fibroin and sericin induced c-Jun transcription and phosphorylation are prevented by JNK, PI3K or MEK inhibitors.

Figure 6

For A and B, serum-deprived, sub-confluent MDA-MB-231 cells were treated for different times with either 0.4% fibroin or 0.05% sericin in the absence or presence of the following inhibitors: SP600125, LY294002, SB431542 and Y-27632. A. Fibroin treated total cell lysates were analyzed by Western blot for phospho-ERK1/2, c-Jun, phospho-c-Jun, phospho-JNK1/2 proteins. ß-Actin was used as a protein loading control. B. Sericin treated total cell lysates were analyzed by Western blot for phospho-ERK1/2, c-Jun, phospho-c-Jun, phospho-JNK1/2 proteins. ß-Actin was used as a protein loading control. For C and D, serum-deprived, sub-confluent MDA-MB-231 cells were treated for different times with either 0.4% fibroin or 0.05% sericin in the absence or presence of the following inhibitors: SP600125 and PD98059. C. Fibroin treated total cell lysates were analyzed by Western blot for phospho-ERK1/2, c-Jun, phospho-c-Jun, phospho-JNK1/2 proteins. ß-Actin was used as a protein loading control. D. Sericin treated total cell lysates were analyzed by Western blot for phospho-ERK1/2, c-Jun, phospho-c-Jun, phospho-JNK1/2 proteins. ß-Actin was used as a protein loading control.