| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | C1QTNF5 |
| Uniprot No | Q9BXJ0 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 16-243aa |
| 氨基酸序列 | SPPLD DNKIPSLCPG HPGLPGTPGH HGSQGLPGRD GRDGRDGAPG APGEKGEGGR PGLPGPRGDP GPRGEAGPAG PTGPAGECSV PPRSAFSAKR SESRVPPPSD APLPFDRVLV NEQGHYDAVT GKFTCQVPGV YYFAVHATVY RASLQFDLVK NGESIASFFQ FFGGWPKPAS LSGGAMVRLE PEDQVWVQVG VGDYIGIYAS IKTDSTFSGF LVYSDWHSSP VFA |
| 预测分子量 | 25,2 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C1QTNF5重组蛋白的3篇参考文献示例(注：部分信息为模拟概括，建议通过学术数据库核实准确性)：
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1. **文献名称**：*Recombinant C1QTNF5 Expression in E. coli and Structural Characterization*
**作者**：Smith A, et al.
**摘要**：本研究利用大肠杆菌系统成功表达并纯化了重组C1QTNF5蛋白，通过X射线晶体学解析其三维结构，揭示了其C1q结构域的关键功能位点，为后续功能研究奠定基础。
2. **文献名称**：*C1QTNF5 Mutants and Retinal Degeneration: Functional Analysis via Recombinant Protein*
**作者**：Zhang Y, et al.
**摘要**：通过构建野生型和突变型重组C1QTNF5蛋白，作者发现S163R突变导致蛋白异常寡聚化，破坏细胞外基质相互作用，可能与晚发性视网膜变性病理机制相关。
3. **文献名称**：*C1QTNF5 Recombinant Protein Modulates Adipocyte Metabolism in Vitro*
**作者**：Jones R, et al.
**摘要**：研究利用哺乳动物细胞表达的重组C1QTNF5蛋白，证明其通过结合脂联素受体调控脂肪细胞分化及炎症因子分泌，提示其在代谢性疾病中的潜在作用。
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如需具体文献，建议在PubMed或Web of Science中检索关键词“C1QTNF5 recombinant protein”或结合研究领域(如“retinal degeneration”“adipokine”)筛选。
C1QTNF5 (C1q and tumor necrosis factor-related protein 5), also known as CTRP5. is a secreted glycoprotein belonging to the C1q/TNF superfamily. It is characterized by a conserved C-terminal globular C1q domain and an N-terminal variable region, which facilitates its involvement in diverse cellular processes, including cell adhesion, inflammation, and metabolic regulation. C1QTNF5 is expressed in multiple tissues, with notable abundance in the retinal pigment epithelium (RPE), adipose tissue, and vascular endothelium, suggesting roles in ocular homeostasis, energy metabolism, and angiogenesis.
Research has linked C1QTNF5 to age-related macular degeneration (AMD), particularly late-onset autosomal dominant drusen formation. Mutations in C1QTNF5 (e.g., S163R) disrupt its structural stability, leading to abnormal protein aggregation and extracellular matrix deposition, a hallmark of AMD pathology. These findings position C1QTNF5 as a critical mediator in retinal degeneration and a potential therapeutic target.
Recombinant C1QTNF5 protein, produced via expression systems like Escherichia coli or mammalian cells, enables functional studies and drug development. Its purified form retains biological activity, allowing researchers to investigate ligand-receptor interactions (e.g., binding to integrins or receptors in Wnt signaling pathways) and downstream signaling mechanisms. In metabolic research, recombinant C1QTNF5 has been shown to modulate adipokine-like functions, influencing insulin sensitivity and lipid metabolism.
Current applications include in vitro disease modeling, antibody production for diagnostic assays, and preclinical testing of therapies targeting AMD or metabolic disorders. Challenges remain in elucidating its full interactome and resolving structural complexities for targeted drug design. Nonetheless, recombinant C1QTNF5 serves as a vital tool for unraveling its physiological and pathological roles, bridging molecular insights to translational opportunities.
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