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Intriguingly, the interactions of N-terminal histidine residues of the prion protein (PrP) mainly with Cu 2+ sequestration and accumulation in diseased brain (T 2+ at neutral pH (7.4) ( 2+ is not necessarily pathogenic since it has also been found to produce neuroprotection due to the cis interaction with the C terminal of PrP

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Combining these peptides enables researchers to investigate GH-axis signaling integration and receptor-level pathway coordination