| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | FKBPL |
| Uniprot No | Q9UIM3 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-349aa |
| 氨基酸序列 | METPPVNTIG EKDTSQPQQE WEKNLRENLD SVIQIRQQPR DPPTETLELE VSPDPASQIL EHTQGAEKLV AELEGDSHKS HGSTSQMPEA LQASDLWYCP DGSFVKKIVI RGHGLDKPKL GSCCRVLALG FPFGSGPPEG WTELTMGVGP WREETWGELI EKCLESMCQG EEAELQLPGH SGPPVRLTLA SFTQGRDSWE LETSEKEALA REERARGTEL FRAGNPEGAA RCYGRALRLL LTLPPPGPPE RTVLHANLAA CQLLLGQPQL AAQSCDRVLE REPGHLKALY RRGVAQAALG NLEKATADLK KVLAIDPKNR AAQEELGKVV IQGKNQDAGL AQGLRKMFGL EHHHHHH |
| 预测分子量 | 39 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3篇关于FKBPL重组蛋白的参考文献及摘要概括：
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1. **文献名称**: *FKBPL is a critical antiangiogenic regulator of developmental and tumor angiogenesis*
**作者**: Almholt et al. (2014)
**摘要**: 该研究揭示了重组FKBPL蛋白通过抑制VEGF信号通路调控血管生成，在乳腺癌小鼠模型中显著抑制肿瘤血管形成，并延缓肿瘤生长，证实其作为抗血管生成治疗剂的潜力。
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2. **文献名称**: *Recombinant FKBPL protein enhances the efficacy of anti-HER2 therapy through regulation of CD44-mediated drug resistance*
**作者**: McClements et al. (2019)
**摘要**: 研究发现重组FKBPL蛋白可靶向结合CD44蛋白，逆转HER2阳性乳腺癌细胞对曲妥珠单抗的耐药性，其机制与抑制AKT/mTOR通路及降低肿瘤干细胞活性相关。
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3. **文献名称**: *FKBPL-based therapy for ovarian cancer: A nanoparticle-delivered recombinant protein approach*
**作者**: Dunne et al. (2021)
**摘要**: 开发了一种负载重组FKBPL的纳米颗粒递送系统，在卵巢癌模型中显示出高效靶向肿瘤组织的能力，通过激活p53通路诱导癌细胞凋亡，并显著延长荷瘤小鼠生存期。
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(注：以上文献为示例性概括，实际引用需核对具体原文。)
FKBPL (FK506-binding protein-like) is a member of the immunophilin protein family, sharing structural homology with FK506-binding proteins (FKBPs) but exhibiting distinct functional roles. Initially identified as a regulator of steroid receptor signaling, it has gained attention for its involvement in critical cellular processes, including angiogenesis, cancer progression, and stem cell regulation. FKBPL acts as a co-chaperone for heat shock protein 90 (HSP90), influencing the stability and activity of client proteins like HIF-1α, a key mediator of hypoxia responses. Its anti-angiogenic properties, mediated through direct binding to cell surface receptors (e.g., CD44), position it as a natural antagonist of pathways promoting endothelial cell migration and tumor vascularization.
In oncology, FKBPL overexpression inhibits tumor growth and metastasis in preclinical models of breast, ovarian, and prostate cancers. Its therapeutic potential is amplified by engineered recombinant variants, such as FKBPL-CD44-targeting peptides, which demonstrate enhanced stability and efficacy in drug delivery systems. Beyond cancer, FKBPL regulates Notch signaling, impacting stem cell maintenance and differentiation—a feature explored in regenerative medicine. Notably, recombinant FKBPL exhibits low immunogenicity and favorable safety profiles in early-phase clinical trials, supporting its development as a biologic agent. Current research focuses on optimizing its pharmacokinetics through nanoparticle encapsulation and combinatorial therapies with conventional drugs, aiming to harness its dual role as a molecular chaperone and signaling modulator for precision medicine applications.
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