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. 2015 May 27;11(7):975–994. doi: 10.1080/15548627.2015.1049800

Figure 1.

Figure 1.

RIPK1 is upregulated in human melanoma cells under ER stress induced by TM or TG. (A) Whole cell lysates from Mel-RM and MM200 cells with or without treatment with tunicamycin (TM) (3 μM) (left panel) or thapsigargin (TG) (1 μM) (right panel) for the indicated periods were subjected to western blot analysis of RIPK1, HSPA5, and GAPDH (as a loading control). The numbers represent fold changes of HSPA5. The data shown are representative of 3 individual experiments. (B) Total RNA from Mel-RM and MM200 cells with or without treatment with TM (3 μM) (left panel) or TG (1 μM) (right panel) for the indicated periods were subjected to qPCR analysis of RIPK1 mRNA expression. The relative abundance of the RIPK1 mRNA before treatment was arbitrarily designated as 1 (n = 3, mean ±SEM). (C) Total RNA from Mel-RM and MM200 cells treated with TM (3 μM) or TG (1 μM) for 16 h followed by treatment with actinomycin D (100 ng/ml) for the indicated period was subjected to qPCR analysis for the expression of RIPK1 mRNA. The relative abundance of the RIPK1 mRNA without actinomycin D treatment was arbitrarily designated as 1 (n = 3, mean ±SEM, *P < 0.05, Student t test). (D) Whole cell lysates from ME4405, Sk-Mel-28, Mel-CV, IgR3 and Mel-RMu melanoma cells and HEMn-MP melanocytes treated with TM (3 μM) or TG (1 μM) for 16 h were subjected to western blot analysis of RIPK1, HSPA5, and GAPDH (as a loading control). The numbers represent fold changes of HSPA5. The data shown are representative of 3 individual experiments.