Fig. 3From: PERK induces resistance to cell death elicited by endoplasmic reticulum stress and chemotherapyPERK expression in cells resistant to chemotherapy and to ER stress. a, b. Relative expression of 83 UPR genes in untreated HT29/Tun vs. HT29 cells (a), and in untreated HT29/MDR vs. HT29 cells (b). The Volcano plots are representative of 4 independent experiments. The spots corresponding to PERK are encircled. c. Immunoblots of the indicated proteins in extracts of untreated cells. β-tubulin was used as a loading control. The figure is representative of 3 experiments with similar results. d. Nrf2 mRNA levels in extracts of untreated cells. Data are mean ± SD (n = 4). *p < 0.005 vs. HT29 cells. e. Immunoblot of Nrf2 in nuclear extracts of the indicated cells. TATA-box binding protein (TBP) served as a loading control. The figure is representative of 3 experiments with similar results. f. Binding of Nrf2 to the ABCC1/MRP1 promoter (ABCC1 pro) as measured by ChIP. The figure is representative of 3 experiments with similar results. Amplification of ABCC1 promoter from genomic DNA (input) was used as control of equal DNA loading. No Ab: HT29/MDR DNA fragments were immunoprecipitated without the anti-Nrf2 antibody and used as a negative controlBack to article page