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This switch promotes citrate-dependent histone acetylation via ACLY-KAT2A interactions at exhaustion signature genes, while reducing acetate-dependent acetylation, mediated by a p300-ACSS2 complex, at effector and memory gene loci

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Although the mechanism for this effect was not investigated, it could be speculated that GHK-Cu might be triggering a wound healing effect similar to that occurring in damaged skin [13]