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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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Eur J Vasc Endovasc Surg
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11d and 11g) Given the differentiation in conformational dynamics of Cagri-bound versus rAmy-bound to CTR or AMYRs and the likely role that the P37 Cagri played in these differences, we also assessed in the assay an analogue of Cagri that contained a P37Y substitution
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