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This interaction involves: Multiple hydrogen bond formations with ASP-111, VAL-175, and HIS-126 residues Salt bridge and pi-pi stacking interactions supporting binding stability Potential activation of cellular anti-aging pathways independent of muscle effects Antioxidant activity through SIRT1-mediated cellular protection mechanisms This dual mechanism suggests Syn-AKE may influence both immediate muscle activity and longer-term cellular aging processes

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However, the signal transduction pathway, whereby changes in intracellular ATP alter the activity of GI neurons, is completely different

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