| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | DCAF4 |
| Uniprot No | Q8WV16 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-495aa |
| 氨基酸序列 | MNKSRWQSRRRHGRRSHQQNPWFRLRDSEDRSDSRAAQPAHDSGHGDDESPSTSSGTAGTSSVPELPGFYFDPEKKRYFRLLPGHNNCNPLTKESIRQKEMESKRLRLLQEEDRRKKIARMGFNASSMLRKSQLGFLNVTNYCHLAHELRLSCMERKKVQIRSMDPSALASDRFNLILADTNSDRLFTVNDVKVGGSKYGIINLQSLKTPTLKVFMHENLYFTNRKVNSVCWASLNHLDSHILLCLMGLAETPGCATLLPASLFVNSHPGIDRPGMLCSFRIPGAWSCAWSLNIQANNCFSTGLSRRVLLTNVVTGHRQSFGTNSDVLAQQFALMAPLLFNGCRSGEIFAIDLRCGNQGKGWKATRLFHDSAVTSVRILQDEQYLMASDMAGKIKLWDLRTTKCVRQYEGHVNEYAYLPLHVHEEEGILVAVGQDCYTRIWSLHDARLLRTIPSPYPASKADIPSVAFSSRLGGSRGAPGLLMAVGQDLYCYSYS |
| 预测分子量 | 71.7 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DCAF4重组蛋白的3篇模拟参考文献示例(注：部分信息为假设性概括，实际文献需通过学术数据库核实)：
---
1. **文献名称**: *DCAF4 interacts with CUL4-DDB1 ubiquitin ligase complex and regulates substrate recognition*
**作者**: Li, X., Zhang, Y., & Chen, W.
**摘要**: 本研究利用重组表达的DCAF4蛋白，解析其与CUL4-DDB1复合体的结合机制，发现DCAF4作为接头蛋白参与底物识别，并通过体外泛素化实验验证其对特定肿瘤抑制蛋白的靶向降解作用。
2. **文献名称**: *Structural characterization of recombinant DCAF4 and its role in DNA damage response*
**作者**: Sato, K., et al.
**摘要**: 通过大肠杆菌系统表达并纯化DCAF4重组蛋白，结合X射线晶体学揭示其WD40结构域的三维构象。实验表明DCAF4在DNA损伤修复中通过调控CRL4复合体的活性影响细胞周期进程。
3. **文献名称**: *DCAF4 knockdown and recombinant rescue experiments reveal its oncogenic potential in glioblastoma*
**作者**: Wang, H., Liu, T., & Zhou, M.
**摘要**: 在胶质母细胞瘤模型中，通过重组DCAF4蛋白回补实验证明其过表达可激活Wnt/β-catenin信号通路，促进肿瘤细胞侵袭，提示DCAF4作为潜在治疗靶点。
---
**提示**：实际文献建议通过PubMed、Google Scholar或Web of Science检索关键词"DCAF4 recombinant protein"或"DCAF4 AND CRL4 complex"，筛选近5年涉及蛋白表达、结构或功能研究的论文。
**Background of DCAF4 Recombinant Protein**
DCAF4 (DDB1- and CUL4-associated factor 4) is a substrate recognition component within the CUL4-DDB1 E3 ubiquitin ligase complex, which plays a critical role in the ubiquitin-proteasome system. This system governs targeted protein degradation, a process essential for regulating cellular processes such as DNA repair, cell cycle progression, and stress responses. DCAF4 contains a conserved WD40 repeat domain, enabling it to interact with specific substrates and recruit them to the E3 ligase machinery for ubiquitination and subsequent degradation.
The recombinant form of DCAF4 is engineered for experimental studies to elucidate its biological functions and mechanisms. Produced via heterologous expression systems (e.g., *E. coli* or mammalian cells), recombinant DCAF4 retains its ability to bind DDB1 and participate in ubiquitination cascades. Researchers utilize this protein to investigate its role in diseases, particularly cancer, where dysregulation of ubiquitin-mediated proteolysis is often implicated. For example, DCAF4 has been linked to pathways involving tumor suppressors or oncoproteins, suggesting its potential as a therapeutic target.
Additionally, DCAF4 recombinant protein is employed in structural studies to map interaction interfaces or screen for small-molecule modulators. Its applications extend to *in vitro* ubiquitination assays, protein interaction analyses, and functional genomics. Despite progress, many aspects of DCAF4’s biology, including its full substrate repertoire and tissue-specific roles, remain underexplored. Ongoing research aims to uncover its regulatory networks and therapeutic relevance in precision medicine.
In summary, DCAF4 recombinant protein serves as a vital tool for dissecting the molecular mechanisms of ubiquitin-dependent protein turnover and its implications in health and disease.
×
