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Subsequent studies indicated that protein kinase A (PKA), protein kinase C (PKC) and Ca 2+ /calmodulin-dependent kinase II (CKII) could each phosphorylate the catalytic subunit of GCL in vitro , resulting in an approximately 20% reduction in V max (Sun et al., 1996)

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On one hand, activity at such vanishingly small concentrations is consistent with GHK-Cu’s proposed role as a physiological signaling molecule rather than a blunt pharmacological agent, which is genuinely intriguing