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Copper ion binding/sequestration denotes the ability of various proteins—including prion protein (PrP), copper chaperones (e.g., CopZ), metalloproteins (e.g., MbnP, MopE*, CorA)—to specifically bind and control copper ions through conserved motifs such as histidine- and methionine-rich sequences[1][2][5]. These proteins regulate copper availability for cellular processes, protect against oxidative damage, and are critical for enzymatic activities and structural integrity[6]. Dysregulation of copper binding is linked to neurodegenerative diseases, infection susceptibility, and metabolic disorders[3][6][1]. The term refers to a function; to study a specific therapeutic target, an individual copper-binding protein or its gene should be identified.
Chelation and removal of copper ions\nModulation of copper-binding affinity\nInhibition or stabilization of copper-binding proteins\nRestoration or suppression of copper-dependent enzymatic activity
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