人 CD42b 抗体对
01AB00512
Glycoprotein Ib platelet subunit alpha (GP1BA) is a protein that plays a crucial role in blood clotting. It is part of the GPIb-IX-V complex, which is found on the surface of platelets and acts as a receptor for von Willebrand factor (VWF). This interaction facilitates the initial adhesion of platelets to the vascular subendothelium after vascular injury, leading to enhanced platelet activation, thrombosis, and hemostasis. Mutations in the GP1BA gene can cause bleeding disorders such as Bernard-Soulier syndrome and platelet-type von Willebrand disease. Bernard-Soulier syndrome is characterized by a reduced number of larger-than-normal platelets (macrothrombocytopenia) and excessive bleeding, while platelet-type von Willebrand disease involves excessive binding of the GPIb-IX-V complex to VWF, leading to mild bleeding abnormalities.
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技术参数
- 靶点基因名
- GP1BA
- 蛋白别名
- glycoprotein Ib platelet subunit alpha; CD42b
- UniProt
- P07359
- 物种
- Human
产品详情
- 靶点名称
- CD42b
- 蛋白名称
- glycoprotein Ib platelet subunit alpha
- 蛋白别名
- Platelet glycoprotein Ib alpha chain; GP-Ib alpha; GPIb-alpha; GPIbA; Glycoprotein Ibalpha; Antigen CD42b-alpha; CD antigen CD42b) [Cleaved into: Glycocalicin]
- 靶点基因名
- GP1BA
- UniProt
- P07359
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Glycoprotein Ib platelet subunit alpha (GP1BA) is a protein that plays a crucial role in blood clotting. It is part of the GPIb-IX-V complex, which is found on the surface of platelets and acts as a receptor for von Willebrand factor (VWF). This interaction facilitates the initial adhesion of platelets to the vascular subendothelium after vascular injury, leading to enhanced platelet activation, thrombosis, and hemostasis. Mutations in the GP1BA gene can cause bleeding disorders such as Bernard-Soulier syndrome and platelet-type von Willebrand disease. Bernard-Soulier syndrome is characterized by a reduced number of larger-than-normal platelets (macrothrombocytopenia) and excessive bleeding, while platelet-type von Willebrand disease involves excessive binding of the GPIb-IX-V complex to VWF, leading to mild bleeding abnormalities.