抗人 EVL 抗体对
01AB02411
Enah/Vasp-like (EVL) is a member of the Ena/VASP protein family, characterized by its modular structure comprising an EVH1 domain for membrane targeting and an EVH2 domain containing G-actin and F-actin binding sites, as well as a coiled-coil motif essential for tetramerization and actin filament bundling. EVL localizes to the leading edge of lamellipodia and filopodial tips, where it regulates actin dynamics by promoting actin polymerization and inhibiting filament capping, thereby facilitating cellular processes such as shape change, adhesion, migration, and cell-cell interaction. The EVH2 domain is crucial for actin binding and polymerization, with specific motifs mediating interactions with actin monomers and filaments, and phosphorylation sites modulating its activity. Dysregulation of EVL and related Ena/VASP proteins has been implicated in diseases including thrombosis, cancer, arteriosclerosis, cardiomyopathy, and nephritis, highlighting their significance in both cellular homeostasis and pathology.
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技术参数
- 靶点基因名
- EVL
- 基因别名
- RNB6
- 蛋白别名
- Enah/Vasp-like; EVL
- UniProt
- Q9UI08
- 物种
- Human
产品详情
- 靶点名称
- EVL
- 蛋白名称
- Enah/Vasp-like
- 蛋白别名
- Ena/VASP-like protein; Ena/vasodilator-stimulated phosphoprotein-like
- 靶点基因名
- EVL
- 基因别名
- RNB6
- UniProt
- Q9UI08
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Enah/Vasp-like (EVL) is a member of the Ena/VASP protein family, characterized by its modular structure comprising an EVH1 domain for membrane targeting and an EVH2 domain containing G-actin and F-actin binding sites, as well as a coiled-coil motif essential for tetramerization and actin filament bundling. EVL localizes to the leading edge of lamellipodia and filopodial tips, where it regulates actin dynamics by promoting actin polymerization and inhibiting filament capping, thereby facilitating cellular processes such as shape change, adhesion, migration, and cell-cell interaction. The EVH2 domain is crucial for actin binding and polymerization, with specific motifs mediating interactions with actin monomers and filaments, and phosphorylation sites modulating its activity. Dysregulation of EVL and related Ena/VASP proteins has been implicated in diseases including thrombosis, cancer, arteriosclerosis, cardiomyopathy, and nephritis, highlighting their significance in both cellular homeostasis and pathology.