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Blood, Vol. 112, Issue 6, 2450-2462, September 15, 2008 This Article Abstract Full Text Services Email this article to a friend Alert me to new issues of the journal Rights and Permissions Citing Articles Citing Articles via CrossRef Targeting MEK/MAPK signal transduction module potentiates ATO-induced apoptosis in multiple myeloma cells through multiple signaling pathways Blood Lunghi et al. 112: 2450 Supplemental materials for: Lunghi et al Files in this Data Supplement: Document 1. Supplemental materials and methods (PDF, 79.5 KB) Figure S1. Either PD325901 (50 nM) or PD184352 (1 µM) completely suppress ERK phosphorylation and activate caspase-3 when combined with ATO (JPG, 109 KB) - MM cells were seeded at 2.5 × 105 cells/mL in the presence of DMSO (vehicle) PD325901 (50 nM) or PD184352 (1 µM) for 3 hours and then were incubated for 24 hours with ATO (2 µM), after which cells were lysed and subjected to Western blot analysis to monitor the expression of Cleaved caspase-3, phospho-ERK1/2, ERK1/2, Bim and actin. PD325901 (50nM), a second generation non-competitive with ATP inhibitor of MEK, causes downregulation of p-ERK and upregulation of Bim but at 20 fold lower concentrations of drug than PD184352 (1 µM). As observed with PD184352 (1 µM) plus ATO combination, PD325901 (50nM) plus ATO (2 µM) activates caspase-3 in MM cells. This Article Abstract Full Text Services Email this article to a friend Alert me to new issues of the journal Rights and Permissions Citing Articles Citing Articles via CrossRef

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