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Notably, we have revealed here that sustained intracellular GSH levels are essential for CD8 + T cell expansion, survival, and effector function and defined the complete dependence of such regulation on GPX4 expression and activity, through a metabolic signaling axis that ties the A2AR/PKA/E2F1 pathway to GSH metabolism and lipid peroxidation

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HDAC inhibition leads to a more permissive chromatin state, enhancing transcription of genes involved in neuronal survival, synaptic plasticity, and memory formation [106]