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人铜蓝蛋白抗体对
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人铜蓝蛋白抗体对

01AB01075

Ceruloplasmin (CP) is a blue, multicopper-binding glycoprotein and the primary copper-carrying protein in human plasma, responsible for transporting over 95% of plasma copper and playing a crucial role in iron metabolism through its ferroxidase activity, which oxidizes Fe(2+) to Fe(3+) without generating harmful radical oxygen species. Structurally, ceruloplasmin contains a mononuclear copper site and a tricopper center, enabling it to transfer electrons and facilitate the safe loading of ferric iron into transferrin, thus preventing oxidative damage and supporting antioxidant defense. Beyond copper and iron transport, ceruloplasmin interacts with proteins such as ferritin, ferroportin 1, and lactoferrin, and is involved in neural transmission, inflammation regulation, and blood clotting. Clinically, loss-of-function mutations in the CP gene can cause aceruloplasminemia, a rare neurodegenerative disorder characterized by iron accumulation in tissues, while ceruloplasmin deficiency is also implicated in Wilson disease and other disorders of copper metabolism.

Human
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技术参数

靶点基因名
CP
蛋白别名
ceruloplasmin; Ceruloplasmin
UniProt
P00450
物种
Human

产品详情

靶点名称
Ceruloplasmin
蛋白名称
ceruloplasmin
蛋白别名
Ceruloplasmin; Ferroxidase
靶点基因名
CP
UniProt
P00450
来源物种
Homo sapiens (Human)
物种反应性
Human

背景介绍

Ceruloplasmin (CP) is a blue, multicopper-binding glycoprotein and the primary copper-carrying protein in human plasma, responsible for transporting over 95% of plasma copper and playing a crucial role in iron metabolism through its ferroxidase activity, which oxidizes Fe(2+) to Fe(3+) without generating harmful radical oxygen species. Structurally, ceruloplasmin contains a mononuclear copper site and a tricopper center, enabling it to transfer electrons and facilitate the safe loading of ferric iron into transferrin, thus preventing oxidative damage and supporting antioxidant defense. Beyond copper and iron transport, ceruloplasmin interacts with proteins such as ferritin, ferroportin 1, and lactoferrin, and is involved in neural transmission, inflammation regulation, and blood clotting. Clinically, loss-of-function mutations in the CP gene can cause aceruloplasminemia, a rare neurodegenerative disorder characterized by iron accumulation in tissues, while ceruloplasmin deficiency is also implicated in Wilson disease and other disorders of copper metabolism.