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When serine and threonine residues within the ΔC truncation were replaced by alanine (Sec24C MUT), VRK2 could not increase phosphorylation of Sec24C MUT (Fig

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So the current hypothesis regarding the mechanism of amyloid β -stimulated oxidative damage in cells is that amyloid β directly interacts with catalase by binding with the protein and deactivating its catalytic activity thereby creating oxidative stress conditions