| 纯度 | >95%SDS-PAGE. |
| 种属 | Human |
| 靶点 | Flt3 |
| Uniprot No | P49771 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 27-184aa |
| 氨基酸序列 | TQDCSFQHSPISSDFAVKIRELSDYLLQDYPVTVASNLQDEELCGALWRL VLAQRWMERLKTVAGSKMQGLLERVNTEIHFVTKCAFQPPPSCLRFVQTN ISRLLQETSEQLVALKPWITRQNFSRCLELQCQPDSSTLPPPWSPRPLEA TAPTAPQP |
| 预测分子量 | 18 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篇参考文献及其摘要概括：
1. **《Structural and functional analysis of the Flt3 ligand》**
- 作者：Griffith, J., et al.
- 摘要：通过X射线晶体学解析Flt3配体(重组蛋白)的三维结构，揭示其与Flt3受体结合的分子机制，为靶向治疗提供结构基础。
2. **《Flt3 ligand synergizes with granulocyte colony-stimulating factor to mobilize hematopoietic progenitor cells》**
- 作者：Brasel, K., et al.
- 摘要：研究重组Flt3配体与G-CSF联用对造血干细胞动员的影响，证实其协同作用可显著增强外周血干细胞的增殖与迁移。
3. **《Flt3 mutations in acute myeloid leukemia: therapeutic implications》**
- 作者：Small, D., et al.
- 摘要：分析Flt3受体酪氨酸激酶结构域突变(如ITD)在白血病中的作用，并探讨重组蛋白抑制剂在体外模型中的抗肿瘤效果。
4. **《Expression and purification of recombinant Flt3 extracellular domain in mammalian cells》**
- 作者：Larsson, A., et al.
- 摘要：描述利用哺乳动物表达系统高效生产可溶性Flt3胞外域重组蛋白的方法，优化纯化流程并验证其生物活性(如配体结合能力)。
以上文献涵盖Flt3重组蛋白的结构解析、功能研究、突变关联疾病及生产方法，均为该领域经典研究方向。
**Background of FLT3 Recombinant Protein**
FLT3 (FMS-like tyrosine kinase 3), also known as CD135. is a member of the class III receptor tyrosine kinase (RTK) family, which includes receptors like KIT, PDGFR, and CSF1R. It plays a critical role in hematopoiesis, particularly in the development, survival, and differentiation of hematopoietic stem cells (HSCs) and progenitor cells. FLT3 is predominantly expressed in bone marrow, lymphoid tissues, and the placenta. Its activation occurs upon binding to its ligand, FLT3 ligand (FLT3L), leading to dimerization, autophosphorylation, and downstream signaling through pathways such as PI3K/AKT, RAS/MAPK, and STAT5. These pathways regulate cell proliferation, apoptosis resistance, and lineage commitment.
Dysregulation of FLT3 signaling is strongly linked to hematologic malignancies. Activating mutations in FLT3. particularly internal tandem duplications (FLT3-ITD), are found in ~30% of acute myeloid leukemia (AML) cases and correlate with poor prognosis. These mutations cause constitutive kinase activity, driving uncontrolled cell growth. Consequently, FLT3 has emerged as a therapeutic target, with inhibitors like midostaurin and gilteritinib approved for AML treatment.
Recombinant FLT3 protein is engineered *in vitro* using expression systems (e.g., mammalian, insect, or bacterial cells) to produce soluble forms, often comprising the extracellular domain or kinase domain. This protein serves as a vital tool for *in vitro* studies, including ligand-receptor interaction assays, structural analysis, and drug screening. It also aids in developing monoclonal antibodies or targeted therapies. By enabling precise investigation of FLT3’s function and inhibition, recombinant FLT3 protein supports both basic research and translational efforts to combat FLT3-driven malignancies.
(Word count: 249)
×
