| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | ACKR3 |
| Uniprot No | P25106 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-362aa |
| 氨基酸序列 | MDLHLFDYSEPGNFSDISWPCNSSDCIVVDTVMCPNMPNKSVLLYTLSFIYIFIFVIGMIANSVVVWVNIQAKTTGYDTHCYILNLAIADLWVVLTIPVWVVSLVQHNQWPMGELTCKVTHLIFSINLFGSIFFLTCMSVDRYLSITYFTNTPSSRKKMVRRVVCILVWLLAFCVSLPDTYYLKTVTSASNNETYCRSFYPEHSIKEWLIGMELVSVVLGFAVPFSIIAVFYFLLARAISASSDQEKHSSRKIIFSYVVVFLVCWLPYHVAVLLDIFSILHYIPFTCRLEHALFTALHVTQCLSLVHCCVNPVLYSFINRNYRYELMKAFIFKYSAKTGLTKLIDASRVSETEYSALEQSTK |
| 预测分子量 | 41,4 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ACKR3重组蛋白的3篇代表性文献及其摘要(文献信息为示例性概括)：
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1. **标题**: *Structural basis of ACKR3 activation by CC chemokine ligand 2*
**作者**: Smith A, et al.
**摘要**: 通过冷冻电镜解析ACKR3与配体CCL2结合的复合物结构，揭示了受体胞外域构象变化及下游β-arrestin信号激活机制，为设计靶向ACKR3的炎症性疾病药物提供结构基础。
2. **标题**: *ACKR3 regulates breast cancer metastasis via HIF-1α/VEGF pathway*
**作者**: Zhang L, et al.
**摘要**: 研究证明ACKR3重组蛋白在乳腺癌细胞中通过稳定HIF-1α增强VEGF表达，促进血管生成和肿瘤转移，靶向ACKR3可抑制小鼠模型中肿瘤扩散。
3. **标题**: *Biased signaling of ACKR3: Interactions with CXCR4 and β-arrestin*
**作者**: Jones R, et al.
**摘要**: 利用重组ACKR3蛋白发现其与CXCR4形成异源二聚体，并通过β-arrestin介导非典型信号转导，揭示其在干细胞归巢和免疫调节中的双重功能。
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**备注**：以上内容为领域研究方向的概括性示例，实际文献需通过PubMed或Web of Science等平台检索关键词“ACKR3 recombinant protein”获取。
ACKR3 (Atypical Chemokine Receptor 3), formerly known as CXCR7. is a member of the G protein-coupled receptor (GPCR) family but classified as a "decoy" or scavenging receptor due to its atypical signaling properties. Unlike canonical chemokine receptors, ACKR3 does not activate G protein-mediated pathways upon ligand binding. Instead, it regulates chemokine bioavailability by internalizing ligands like CXCL12 (SDF-1) and CXCL11. modulating their spatial distribution and downstream cellular responses. This unique mechanism positions ACKR3 as a critical player in immune regulation, embryonic development, and disease progression, particularly in cancer metastasis and inflammatory disorders.
Recombinant ACKR3 proteins are engineered in vitro using expression systems (e.g., mammalian cells, insect cells) to produce functional receptor domains or full-length proteins for research. These proteins retain key structural features, including the seven transmembrane helices and ligand-binding regions, enabling studies on receptor-ligand interactions, signaling crosstalk, and drug discovery. Researchers utilize recombinant ACKR3 to investigate its β-arrestin-dependent signaling pathways, which influence cell migration, survival, and angiogenesis. Its overexpression in tumors, often linked to therapy resistance, has spurred interest in developing ACKR3-targeted therapeutics. Recombinant forms are also essential for structural studies (e.g., cryo-EM) to resolve binding motifs and design inhibitors. Despite lacking classical GPCR signaling, ACKR3's role in scavenging chemokines and forming heterodimers with other receptors (e.g., CXCR4) makes it a multifaceted regulator in physiological and pathological contexts.
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