人 CD105 抗体对
01AB03681
Endoglin (ENG), also known as CD105, is a type I membrane glycoprotein primarily associated with human vascular endothelium. It is part of the TGF-beta receptor complex and plays a crucial role in angiogenesis, which is essential for tumor growth, survival, and metastasis of cancer cells. Structurally, endoglin consists of a homodimer of 180 kDA stabilized by intermolecular disulfide bonds, with a large extracellular domain, a hydrophobic transmembrane domain, and a short cytoplasmic tail. Functionally, it acts as an auxiliary receptor for the TGF-beta receptor complex, modulating responses to TGF-beta1, TGF-beta3, activin-A, BMP-2, BMP-7, and BMP-9, and is involved in cytoskeletal organization, affecting cell morphology and migration. Mutations in the ENG gene are associated with hereditary hemorrhagic telangiectasia type 1 (HHT1), a disorder characterized by vascular malformations and bleeding. The protein's expression is regulated during heart development, and experimental mice lacking the endoglin gene die due to cardiovascular abnormalities.
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|---|---|
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技术参数
- 靶点基因名
- ENG
- 基因别名
- END
- 蛋白别名
- endoglin; CD105
- UniProt
- P17813
- 物种
- Human
产品详情
- 靶点名称
- CD105
- 蛋白名称
- endoglin
- 蛋白别名
- Endoglin; CD antigen CD105
- 靶点基因名
- ENG
- 基因别名
- END
- UniProt
- P17813
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Endoglin (ENG), also known as CD105, is a type I membrane glycoprotein primarily associated with human vascular endothelium. It is part of the TGF-beta receptor complex and plays a crucial role in angiogenesis, which is essential for tumor growth, survival, and metastasis of cancer cells. Structurally, endoglin consists of a homodimer of 180 kDA stabilized by intermolecular disulfide bonds, with a large extracellular domain, a hydrophobic transmembrane domain, and a short cytoplasmic tail. Functionally, it acts as an auxiliary receptor for the TGF-beta receptor complex, modulating responses to TGF-beta1, TGF-beta3, activin-A, BMP-2, BMP-7, and BMP-9, and is involved in cytoskeletal organization, affecting cell morphology and migration. Mutations in the ENG gene are associated with hereditary hemorrhagic telangiectasia type 1 (HHT1), a disorder characterized by vascular malformations and bleeding. The protein's expression is regulated during heart development, and experimental mice lacking the endoglin gene die due to cardiovascular abnormalities.