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All rights reserved. http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RADGVS-pHki1MIEI6YVajX98QeKoTNNqJDxQ56dCG1wjU#_6 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RADGVS-pHki1MIEI6YVajX98QeKoTNNqJDxQ56dCG1wjU#_5 http://www.w3.org/ns/prov#value Overexpression of Akt led to upregulation of VEGF, increased production of superoxide ROS, and the switch to a more pronounced glycolytic metabolism ... and ... Second, Akt can induce expression of the ROS-generating enzyme NOX4.... From Full text... We further demonstrated that Akt induced genes associated with resistance to ROS, including Sirt1 and rictor, and activation of the AP-1 subunit JunD.... ....And... Treatment of this spontaneous melanoma with the Akt inhibitor resulted in significant decreases in 3 genes that may account for this resistance. Sirt1 is a deacetylase that attenuates p53 in the presence of oxidative stress; rictor is a rapamycin-insensitive member of the mammalian target of rapamycin complex; and VEGF is likely the major angiogenic factor in melanoma. Inhibition of Akt led to significant and reproducible decreases in the mRNA levels of all 3 genes. .... Note: if they didnt not use an inhibitor to verify AKT action, I coded to expression of AKT. 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