抗人 GAP43 抗体对
01AB01140
Growth Associated Protein 43 (GAP43), also known as neuromodulin or B-50, is a neuron-specific phosphoprotein highly expressed in growth cones during neural development and axonal regeneration, playing a central role in axonal outgrowth, synaptic plasticity, and presynaptic function. GAP43 is a major component of motile growth cones at the tips of elongating axons, where it modulates actin filament dynamics through phosphorylation-dependent mechanisms, acting as a capping protein in its unphosphorylated state and as a lateral stabilizer when phosphorylated, thus influencing filopodial extension and axonal pathfinding. It is tightly regulated at transcriptional, post-transcriptional, and post-translational levels, with protein kinase C-mediated phosphorylation being crucial for its function in neuroplasticity, long-term potentiation, and memory formation. Disease relevance is underscored by the fact that null mutations in GAP43 result in severe axon pathfinding defects and neonatal lethality.
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技术参数
- 靶点基因名
- GAP43
- 蛋白别名
- growth associated protein 43; GAP43
- UniProt
- P17677
- 物种
- Human
产品详情
- 靶点名称
- GAP43
- 蛋白名称
- growth associated protein 43
- 蛋白别名
- Neuromodulin; Axonal membrane protein GAP-43; Growth-associated protein 43; Neural phosphoprotein B-50; pp46
- 靶点基因名
- GAP43
- UniProt
- P17677
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Growth Associated Protein 43 (GAP43), also known as neuromodulin or B-50, is a neuron-specific phosphoprotein highly expressed in growth cones during neural development and axonal regeneration, playing a central role in axonal outgrowth, synaptic plasticity, and presynaptic function. GAP43 is a major component of motile growth cones at the tips of elongating axons, where it modulates actin filament dynamics through phosphorylation-dependent mechanisms, acting as a capping protein in its unphosphorylated state and as a lateral stabilizer when phosphorylated, thus influencing filopodial extension and axonal pathfinding. It is tightly regulated at transcriptional, post-transcriptional, and post-translational levels, with protein kinase C-mediated phosphorylation being crucial for its function in neuroplasticity, long-term potentiation, and memory formation. Disease relevance is underscored by the fact that null mutations in GAP43 result in severe axon pathfinding defects and neonatal lethality.