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Treatment-induced tumor dormancy through YAP-mediated transcriptional reprogramming of the apoptotic pathway

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GHK-Cu treatment reduced reactive oxygen species (ROS) production, increased superoxide dismutase (SOD) activity, and decreased TNF- and IL-6 production by inhibiting NF-B p65 and p38 MAPK signaling in LPS-induced macrophages and ALI models

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