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Specific cysteines in the core domain of mutant p53 proteins are critical targets for their reactivation by APR-246/MQ
It was reported that the GS-ylation of p53 may prevent the formation of the tetramer, and may be involved in oxidative stress conditions and neurodegeneration observed in AD pathogenesis [70]
Additionally, microglia, the brains resident immune cells, exhibit a metabolic flexibility that allows them to shift between oxidative phosphorylation and glycolysis, depending on their activation state, which significantly influences neuroinflammation and synaptic plasticity
albicans was 95.5%
