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It achieves this massive accumulation of monoamines through a combination of several synergistic mechanisms at the presynaptic nerve terminal (Figure 2)

This mechanism underpins its fibroblast migration-promoting effects and helps explain its capacity to accelerate tissue repair at a cellular motility level independent of proliferation

STAT5 promotes PD-L1 expression by facilitating histone lactylation to drive immunosuppression in acute myeloid leukemia

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