. . . . . . . . . . . . . . . "kin(p(PFH:\"AKT Family\")) -> r(HGNC:VEGFA)" . "Approximately 61,000 statements." . "Copyright (c) 2011-2012, Selventa. All rights reserved." . "BEL Framework Large Corpus Document" . . "1.4" . "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. If they used an inhibitor to verify action, coded to kaof (AKT)" . . "Selventa" . . . . "2014-07-03T14:30:49.391+02:00"^^ . . .