<p><b>Copyright information:</b></p><p>Taken from "Cytotoxic effect of 5-aminoimidazole-4-carboxamide-1-β-4-ribofuranoside (AICAR) on childhood acute lymphoblastic leukemia (ALL) cells: implication for targeted therapy"</p><p>http://www.molecular-cancer.com/content/6/1/46</p><p>Molecular Cancer 2007;6():46-46.</p><p>Published online 10 Jul 2007</p><p>PMCID:PMC1948012.</p><p></p> () CCRF-CEM, NALM6, REH, and SupB15 ALL cells treated with 0.25 mM AICAR for the indicated times (0 – 24 h) were analyzed by Western blot for phosphorylated p38-MAPK protein (P-p38-MAPK, Thr180/Tyr182). β-actin was used as a loading control. Density value of each band was normalized to their respective β-actin level and expressed relative to control (untreated). () Cell proliferation assays of CCRF-CEM, NALM6, REH, and SupB15 cells treated with 0.25 mM AICAR alone, 10 μM of the p38-MAPK inhibitor SB 202190 alone (SB), or both agents together (SB + AICAR). The cell proliferation values are expressed as a percentage relative to those obtained with untreated control cells (mean ± SEM, n = 3). Data are representative of at least three independent experiments. *, < 0.01 for AICAR SB + AICAR; #, < 0.05 for AICAR SB + AICAR
