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. 2010 Jul;12(7):527–538. doi: 10.1593/neo.92048

Figure 3.

Figure 3

ATF3 induction by cisplatin is independent of a p53, BRCA1, and ISR mechanism. (A) Schematic representation of the potential mechanisms involved in ATF3 induction by cisplatin. (B) ATF3 detection in PC3 cells transduced with no virus (mock), LacZ vector control (LacZ), or p53wt (p53) containing adenovirus for 6 hours after no treatment (control; top panel) or after treatment with cisplatin (10 µg/ml; middle panel) or taxol (25 µM; bottom panel) for 24 hours. (C) ATF3 expression detected in MCF-7 and 1937 (BRCA1 null) cells untreated (control) or treated with cisplatin (1 and 10 µg/ml) or carboplatin (27 and 270 µg/ml) for 24 hours. (D) ATF3 detection in ATF4-/- and ATF4+/- MEFs untreated (control) or treated with cisplatin (1 µg/ml) and carboplatin (27 µM) for 24 hours. In all blots, actin is used as a loading control.