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The proposed mechanism for the GHK-Cu component is copper chemistry rather than receptor pharmacology: delivery or sequestration of copper relevant to copper-dependent enzymes, and reported changes in extracellular-matrix gene expression in cultured cells
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β-Catenin released from E-cadherin interaction do not translocate directly to the nucleus but to the perinuclear endocytic recycling compartment in A431 cells that express full APC protein (70)
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