Overview
| 别名 | Actin nucleation-promoting factor WAS; Wiskott-Aldrich syndrome protein; WASp |
| 基因名 | WAS |
| UniProt ID | P42768 |
| 反应种属 | Human |
| 应用 | WB |
| 宿主 | Mouse |
| 偶联物 | Unconjugated |
| 修饰 | Unmodified |
| 亚型 | IgG2b |
| 克隆号 | 7W9-N9-C5 |
| 克隆性 | Monoclonal Antibody |
| 分子量 | Calculated MW: 52 kDa |
| 纯化方式 | Affinity Purified |
| 产品形式 | Liquid |
| 推荐稀释比 | WB-1:2000 |
| 存储缓冲液 | Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.09% sodium azide |
| 保存温度 | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
| 背景信息 | The Wiskott-Aldrich Syndrome Protein (WASP) is a key actin nucleation-promoting factor that regulates the dynamics of the actin cytoskeleton through activation of the Arp2/3 complex. WASP facilitates the formation of branched actin filaments, crucial for cellular processes such as endocytosis, cell migration, and immune synapse formation. Its activity is tightly regulated by interactions with Rho-family GTPases and its conserved WH2-Central-Acidic (WCA) domain, which binds actin monomers and the Arp2/3 complex. WASP’s efficiency in actin nucleation varies among family members due to differences in their acidic C-terminal residues, influencing the architecture of actin networks they produce. Mutations in the WAS gene disrupt normal WASP function, leading to diseases like Wiskott-Aldrich Syndrome (WAS), an X-linked disorder characterized by immune deficiencies, thrombocytopenia, and eczema. These mutations often result in unregulated actin polymerization, impairing hematopoietic cell functions and increasing susceptibility to infections. |
检测原理