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Nevertheless, the underlying mechanism governing the upregulation of EAAT3 remains enigmatic

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9, when compared to rats treated with standard pharmaceuticals

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Gln depletion treatment activates FADD and caspase-8-dependent apoptosis involving pro-apoptotic TNF-related apoptosis-inducing ligand receptor 2 (TRAIL-R2) in tumour cells, while metabolic stress induced by glutamine deprivation leads to the downregulation of the GCN2-non-dependent FLICE-inhibitory protein (FLIP), which promotes caspase-8 activation and apoptosis [55]