Activation of AMPK is required for phosphorylation of p38-MAPK in AICAR-treated ALL cells

Abstract

<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> () Immunoblot of p38-MAPK phosphorylation (P-p38-MAPK, Thr180/Tyr182) and β-actin (loading control) expressed in CCRF-CEM and NALM6 cells treated with 0.1% DMSO (Control), 0.5 mM AICAR alone, 0.1 mM iodotubericidin alone (Iodo), or both agents together (Iodo + AICAR). () Phosphorylation status of AMPK (P-AMPK, Thr172) from CCRF-CEM and NALM6 cells incubated with either 0.5 mM AICAR alone, 10 μM SB 202190 alone (SB) or both inhibitors together (SB + AICAR). Level of β-actin was used as loading controls. Density value of each band was normalized to their respective β-actin level and expressed relative to control. The immunoblots shown are representative of 3 independent experiments, which produced similar results

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