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We reasoned that if decreases in glutathione and glutamate in the stable phase are a consequence of damage arising in a preceding acute phase, a sample of stable patients would be more likely to demonstrate a reduction in these neurochemicals than a more heterogeneous sample

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Its primary mechanism involves modulating neurotransmitter systems involved in sleep-wake cycles, particularly GABA and monoamine systems

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Existing evidence suggests that CBP and SIRT4 can promote the ubiquitin-proteasome degradation of BCAT2 by acetylation of BCAT2 at the K44 site in PDAC

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