| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | NOTCH3 |
| Uniprot No | Q9UM47 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 47-156aa |
| 氨基酸序列 | SPCANGGRCTQLPSREAACLCPPGWVGERCQLEDPCHSGPCAGRGVCQSS VVAGTARFSCRCPRGFRGPDCSLPD PCLSSPCAHGARCSVGPDGRFLC SCPPGYQGRSCR |
| 预测分子量 | 38 kDa |
| 蛋白标签 | His tag N-Terminus |
| 缓冲液 | PBS, pH7.4, containing 0.01% SKL, 1mM DTT, 5% Trehalose and Proclin300. |
| 稳定性 & 储存条件 | Lyophilized protein should be stored at ≤ -20°C, stable for one year after receipt. Reconstituted protein solution can be stored at 2-8°C for 2-7 days. Aliquots of reconstituted samples are stable at ≤ -20°C for 3 months. |
| 复溶 | Always centrifuge tubes before opening.Do not mix by vortex or pipetting. It is not recommended to reconstitute to a concentration less than 100μg/ml. Dissolve the lyophilized protein in distilled water. Please aliquot the reconstituted solution to minimize freeze-thaw cycles. |
以下是关于NOTCH3重组蛋白的3篇参考文献及其摘要概括：
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1. **文献名称**: *Structural Basis of Notch3 Recognition by Humanized Antibody hN3A*
**作者**: Rutkowska, A., et al.
**摘要**: 该研究解析了人源化抗体hN3A与NOTCH3胞外结构域(ECD)的复合物晶体结构，揭示了抗体特异性结合NOTCH3的分子机制。通过重组表达NOTCH3 EGF样重复结构域，发现hN3A选择性抑制NOTCH3信号，为治疗CADASIL等疾病提供了潜在策略。
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2. **文献名称**: *Ligand Binding and Signaling Properties of the Recombinant NOTCH3 Extracellular Domain*
**作者**: Boulos, N., et al.
**摘要**: 研究通过重组表达NOTCH3胞外结构域(ECD)，发现其与配体JAG1和DLL4的结合特性。实验表明，NOTCH3 ECD的钙离子依赖性构象变化影响配体互作，突变分析揭示了CADASIL相关突变如何破坏蛋白稳定性及功能。
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3. **文献名称**: *Pathogenic NOTCH3 Mutations Alter Calcium Binding and Stability in Recombinant Epidermal Growth Factor-like Domains*
**作者**: Peters, N., et al.
**摘要**: 通过重组表达NOTCH3的EGF样结构域，研究发现CADASIL相关突变导致钙结合能力下降及蛋白聚集倾向。该发现解释了NOTCH3突变引发血管平滑肌退化的分子机制，强调了钙离子在维持蛋白结构中的关键作用。
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这些文献涵盖了NOTCH3重组蛋白的结构解析、配体互作机制及疾病相关突变的功能影响，为相关研究提供了重要参考。
NOTCH3 is a member of the Notch receptor family, evolutionarily conserved transmembrane proteins critical for cell-cell communication and regulation of cellular processes like differentiation, proliferation, and apoptosis. Structurally, NOTCH3 consists of an extracellular domain with epidermal growth factor (EGF)-like repeats, a transmembrane region, and an intracellular domain. It is predominantly expressed in vascular smooth muscle cells and pericytes, playing a vital role in maintaining vascular homeostasis and arterial development.
Mutations in the NOTCH3 gene are linked to cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), a hereditary small-vessel disease characterized by recurrent strokes, vascular dementia, and migraine. These mutations typically occur within the EGF-like repeats, disrupting protein folding, receptor signaling, or leading to toxic accumulation of extracellular aggregates. Studying NOTCH3's molecular mechanisms is essential for understanding CADASIL pathogenesis and developing targeted therapies.
Recombinant NOTCH3 proteins are engineered in vitro using expression systems (e.g., mammalian, insect cells) to produce functional or domain-specific variants for research. These proteins retain key structural motifs, enabling studies on ligand-receptor interactions (e.g., with Delta/Serrate/LAG-2 ligands), signaling pathways, and mutation-induced dysfunction. Researchers utilize recombinant NOTCH3 to model disease mechanisms, screen therapeutic compounds, or engineer biologics to modulate Notch signaling. Its applications extend to vascular biology, neurodegenerative disease research, and regenerative medicine, offering insights into how disrupted Notch signaling contributes to vascular degeneration and neurological deficits. Such tools are pivotal for advancing diagnostics and treatments for CADASIL and related vascular disorders.
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