人 Antithrombin-III 抗体对
01AB01833
Serpin family C member 1 (SERPINC1) is a glycoprotein serine protease inhibitor (serpin) circulating in plasma that plays a central role in down‑regulating the coagulation cascade by inactivating thrombin and other activated clotting factors such as factors Xa and IXa. Structurally, the mature protein contains a heparin‑binding domain at the N‑terminus and a reactive site loop at the C‑terminus, and binding of heparin induces a conformational change that accelerates its inhibitory activity several‑fold. SERPINC1 shows heparin and protease‑binding activities, participates in hemostasis‑related pathways, and its circulating level and function are essential for maintaining normal anticoagulant balance. Pathologically, more than one hundred SERPINC1 mutations cause quantitative (type I) or qualitative (type II) antithrombin deficiency, a strong hereditary risk factor for venous thrombosis, and reduced antithrombin levels have also been associated with severe thrombophilia and poor outcomes in conditions such as severe COVID‑19.
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技术参数
- 靶点基因名
- SERPINC1
- 基因别名
- AT3
- 蛋白别名
- serpin family C member 1; Antithrombin-III
- UniProt
- P01008
- 物种
- Human
产品详情
- 靶点名称
- Antithrombin-III
- 蛋白名称
- serpin family C member 1
- 蛋白别名
- Antithrombin-III; ATIII; Serpin C1
- 靶点基因名
- SERPINC1
- 基因别名
- AT3
- UniProt
- P01008
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Serpin family C member 1 (SERPINC1) is a glycoprotein serine protease inhibitor (serpin) circulating in plasma that plays a central role in down‑regulating the coagulation cascade by inactivating thrombin and other activated clotting factors such as factors Xa and IXa. Structurally, the mature protein contains a heparin‑binding domain at the N‑terminus and a reactive site loop at the C‑terminus, and binding of heparin induces a conformational change that accelerates its inhibitory activity several‑fold. SERPINC1 shows heparin and protease‑binding activities, participates in hemostasis‑related pathways, and its circulating level and function are essential for maintaining normal anticoagulant balance. Pathologically, more than one hundred SERPINC1 mutations cause quantitative (type I) or qualitative (type II) antithrombin deficiency, a strong hereditary risk factor for venous thrombosis, and reduced antithrombin levels have also been associated with severe thrombophilia and poor outcomes in conditions such as severe COVID‑19.