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Second, there is no obvious theoretical interaction either: the mechanisms described for the Klow components (cytoprotection, actin sequestration, copper-dependent collagen signaling, PepT1-mediated anti-inflammatory action) and the mechanism described for MOTS-c (folate cycle inhibition leading to AMPK activation, with nuclear translocation under metabolic stress) do not converge on a shared receptor, a shared transporter or a shared metabolic bottleneck that would predict competition or potentiation
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