抗人 WASL 抗体对
01AB00699
WASP like actin nucleation promoting factor (WASL), also known as Neural Wiskott-Aldrich Syndrome Protein (N-WASP), is a member of the WASP family that regulates actin cytoskeleton dynamics by activating the Arp2/3 complex, facilitating actin polymerization. Structurally, WASL contains a WASP homology 1 (WH1) domain for binding partners, a basic region (BR), a GTPase-binding domain (GBD), a proline-rich region, and a verprolin-cofilin-acidic (VCA) domain critical for Arp2/3 activation. It integrates signals from Cdc42, phosphoinositides, and SH3 domain-containing proteins to coordinate actin remodeling during processes like endocytosis, cell motility, and neuronal development. Dysregulation of WASL is linked to neurodevelopmental disorders and cancer. Mutations in WASL are associated with X-linked intellectual disability (XLID) and developmental delay, attributed to impaired synaptic plasticity and neurite outgrowth. Additionally, WASL overexpression promotes cancer metastasis by enhancing invasive cell migration.
| 规格 | 起售价 |
|---|---|
| 登录后可查看 | |
技术参数
- 靶点基因名
- WASL
- 蛋白别名
- WASP like actin nucleation promoting factor; WASL
- UniProt
- O00401
- 物种
- Human
产品详情
- 靶点名称
- WASL
- 蛋白名称
- WASP like actin nucleation promoting factor
- 蛋白别名
- Actin nucleation-promoting factor WASL; Neural Wiskott-Aldrich syndrome protein; N-WASP
- 靶点基因名
- WASL
- UniProt
- O00401
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
WASP like actin nucleation promoting factor (WASL), also known as Neural Wiskott-Aldrich Syndrome Protein (N-WASP), is a member of the WASP family that regulates actin cytoskeleton dynamics by activating the Arp2/3 complex, facilitating actin polymerization. Structurally, WASL contains a WASP homology 1 (WH1) domain for binding partners, a basic region (BR), a GTPase-binding domain (GBD), a proline-rich region, and a verprolin-cofilin-acidic (VCA) domain critical for Arp2/3 activation. It integrates signals from Cdc42, phosphoinositides, and SH3 domain-containing proteins to coordinate actin remodeling during processes like endocytosis, cell motility, and neuronal development. Dysregulation of WASL is linked to neurodevelopmental disorders and cancer. Mutations in WASL are associated with X-linked intellectual disability (XLID) and developmental delay, attributed to impaired synaptic plasticity and neurite outgrowth. Additionally, WASL overexpression promotes cancer metastasis by enhancing invasive cell migration.