| 纯度 | >90%SDS-PAGE. |
| 种属 | E.coli |
| 靶点 | FTL3 |
| Uniprot No | Q8VWH2 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-178aa |
| 氨基酸序列 | MAGSGRDDPLVVGRIVGDVLDPFVRITNLSVSYGARIVSNGCELKPSMVTQQPRVVVGGNDMRTFYTLVMVDPDAPSPSNPNLREYLHWLVTDIPGTTGATFGQEVMCYESPRPTMGIHRLVFVLFQQLGRQTVYAPGWRQNFSTRNFAELYNLGSPVATVYFNCQREAGSGGRRVYP |
| 预测分子量 | 19,7 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FLT3重组蛋白的3篇参考文献，涵盖结构、突变机制及治疗应用方向：
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1. **文献名称**：*Structural and mechanistic aspects of FLT3 inhibition*
**作者**：Levis, M., & Small, D. (2003)
**摘要**：该研究解析了FLT3受体酪氨酸激酶的结构特征，利用重组蛋白技术阐明其激活机制，并探讨了ITD突变引起的组成性激活对白血病发生的影响，为靶向药物设计提供结构基础。
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2. **文献名称**：*FLT3 inhibitors as therapeutics for acute myeloid leukemia*
**作者**：Stirewalt, D.L., & Radich, J.P. (2003)
**摘要**：文章综述了FLT3在AML中的突变类型(如ITD/TKD)，通过重组蛋白模型验证突变体的异常信号传导，并评估早期FLT3抑制剂(如米哚妥林)在阻断增殖信号中的效果。
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3. **文献名称**：*Recombinant FLT3 ligand supports leukemia cell growth in vitro*
**作者**：Carow, C.E., et al. (1996)
**摘要**：早期研究证实重组FLT3配体蛋白可促进AML细胞体外增殖，揭示FLT3/FL系统在白血病微环境中的关键作用，为后续靶向治疗策略奠定实验基础。
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**备注**：以上文献年份集中于1990-2000年代，反映FLT3研究的奠基性成果。如需近年研究(如耐药机制或新型重组蛋白药物)，可补充2015年后文献。
**Background of FLT3 Recombinant Protein**
FLT3 (Fms-like tyrosine kinase 3), also known as CD135. is a class III receptor tyrosine kinase primarily expressed on hematopoietic stem and progenitor cells. It plays a critical role in regulating cell survival, proliferation, and differentiation by binding to its ligand, FLT3 ligand (FL). Upon activation, FLT3 triggers downstream signaling pathways, including RAS/MAPK and PI3K/AKT, which are essential for normal hematopoiesis. Dysregulation of FLT3. particularly through mutations such as internal tandem duplications (ITD) or point mutations in the tyrosine kinase domain (TKD), is strongly associated with acute myeloid leukemia (AML). FLT3-ITD mutations, found in ~30% of AML cases, lead to constitutive activation of the receptor, promoting uncontrolled cell growth and poor prognosis.
Recombinant FLT3 proteins are engineered in vitro using expression systems (e.g., mammalian, insect, or bacterial cells) to produce soluble or membrane-bound forms of the receptor or its extracellular domain. These proteins retain functional epitopes and are widely utilized in research to study FLT3 signaling mechanisms, ligand-receptor interactions, and mutation-driven oncogenesis. They also serve as critical tools for drug discovery, enabling the screening and validation of FLT3-targeted inhibitors (e.g., midostaurin, gilteritinib) that block aberrant signaling in AML.
Additionally, FLT3 recombinant proteins are employed in diagnostic assays to detect FLT3 mutations or autoantibodies, aiding in patient stratification and personalized therapy. In immunotherapy, they help develop FLT3-directed CAR-T cells or antibodies to target leukemia cells. The production of high-purity, bioactive FLT3 recombinant proteins ensures reproducibility in both basic and translational studies, contributing to advancements in understanding hematologic malignancies and improving therapeutic outcomes.
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