人 ANGPTL7 抗体对
01AB01431
Angiopoietin like 7 (ANGPTL7) is a secreted glycoprotein of the angiopoietin-like family that functions as a critical regulator of the extracellular matrix (ECM) and angiogenesis. Highly expressed in the corneal stroma, it acts as a negative regulator of blood vessel formation by blocking the Tie2 receptor, thereby maintaining corneal transparency. ANGPTL7 also modulates ECM composition and fibronectin fibrillogenesis, influencing tissue stiffness and remodeling. In pathological contexts, it serves as a pro-fibrotic and pro-inflammatory factor, amplifying TGF-beta signaling and promoting oxidative stress through NF-kappaB activation. Clinically, ANGPTL7 is significantly upregulated in the trabecular meshwork of patients with glaucoma, where it increases aqueous humor outflow resistance and intraocular pressure by driving the formation of cross-linked actin networks.
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技术参数
- 靶点基因名
- ANGPTL7
- 基因别名
- CDT6
- 蛋白别名
- angiopoietin like 7; ANGPTL7
- UniProt
- O43827
- 物种
- Human
产品详情
- 靶点名称
- ANGPTL7
- 蛋白名称
- angiopoietin like 7
- 蛋白别名
- Angiopoietin-related protein 7; Angiopoietin-like factor; Angiopoietin-like protein 7; Cornea-derived transcript 6 protein
- 靶点基因名
- ANGPTL7
- 基因别名
- CDT6
- UniProt
- O43827
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Angiopoietin like 7 (ANGPTL7) is a secreted glycoprotein of the angiopoietin-like family that functions as a critical regulator of the extracellular matrix (ECM) and angiogenesis. Highly expressed in the corneal stroma, it acts as a negative regulator of blood vessel formation by blocking the Tie2 receptor, thereby maintaining corneal transparency. ANGPTL7 also modulates ECM composition and fibronectin fibrillogenesis, influencing tissue stiffness and remodeling. In pathological contexts, it serves as a pro-fibrotic and pro-inflammatory factor, amplifying TGF-beta signaling and promoting oxidative stress through NF-kappaB activation. Clinically, ANGPTL7 is significantly upregulated in the trabecular meshwork of patients with glaucoma, where it increases aqueous humor outflow resistance and intraocular pressure by driving the formation of cross-linked actin networks.