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In addition to using specific inhibitors of the pathways, we used shRNA approaches to simultaneously and specifically knock down Akt-1/2 and BRAF, resulting in synergistic/additive inhibition of melanoma cell proliferation, colony formation and invasion, as well as apoptosis.
However, using specific inhibitors of nitric oxide synthases, we found that iNOS rather than nNOS produced the nitric oxide involved in homeostatic sleep regulation.
In order to understand how ceramide levels increase in response to α-glycoside treatment, further investigations were done using specific inhibitors of sphingolipid metabolic pathways.
By using specific inhibitors of the various cytosolic protein disulfides reducing systems, we show here that the NADPH-thioredoxin reductase-thioredoxin redox system is the main responsible for this disulfide reduction.
Using specific inhibitors of GAT1 and GAT3, NO-711 and SNAP5114, respectively, the ability of FGABAs 1 3 to influence non-GAT1 and non-GAT3 uptake activity of nerve terminals was analyzed, but no specificity was found.
To manipulate the BR levels in plant tissues using specific inhibitors of BR biosynthesis, a series of novel azole derivatives were synthesized and their inhibitory activity on BR biosynthesis was investigated.
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To determine the relative contribution of these TSC kinases to the paracrine mTOR activation by vGPCR, we used specific inhibitors of PI3K/AKT, MEK/ERK, p38 or IKKβ.
To this end, we used specific inhibitors of iNOS and IDO to test whether MSCs from other species also employ either of these two molecules for immunosuppression.
To investigate the regulation of survivin expression in HER-2 induced MCF7 cells we used specific inhibitors of the signal transduction pathways.
Thus, we next used specific inhibitors of p53 and p21 following EZH2-siRNA transfection to clarify the mechanism of modulation of Cdc2 and cyclin B1 expression and cell cycle changes following EZH2 downregulation through the p53 and p21 pathways.
To identify signaling pathways involved in ERK activation, we used specific inhibitors of ERs, epidermal growth factor receptors, Ca2+ signaling, Src and phosphoinositide-3 kinases, and a membrane structure disruption agent.
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