| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | ACKR2 |
| Uniprot No | O00590 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-384aa |
| 氨基酸序列 | MAATASPQPLATEDADSENSSFYYYDYLDEVAFMLCRKDAVVSFGKVFLPVFYSLIFVLGLSGNLLLLMVLLRYVPRRRMVEIYLLNLAISNLLFLVTLPFWGISVAWHWVFGSFLCKMVSTLYTINFYSGIFFISCMSLDKYLEIVHAQPYHRLRTRAKSLLLATIVWAVSLAVSIPDMVFVQTHENPKGVWNCHADFGGHGTIWKLFLRFQQNLLGFLLPLLAMIFFYSRIGCVLVRLRPAGQGRALKIAAALVVAFFVLWFPYNLTLFLHTLLDLQVFGNCEVSQHLDYALQVTESIAFLHCCFSPILYAFSSHRFRQYLKAFLAAVLGWHLAPGTAQASLSSCSESSILTAQEEMTGMNDLGERQSENYPNKEDVGNKSA |
| 预测分子量 | 46.9 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ACKR2重组蛋白的3篇代表性文献的简要总结：
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1. **文献名称**: *ACKR2 regulates dendritic cell migration in inflammation*
**作者**: B. Savino et al.
**摘要**: 本研究通过重组ACKR2蛋白体外实验，发现其通过结合CC类趋化因子(如CCL2、CCL5)调控树突状细胞的迁移。重组ACKR2在炎症模型中表现出对趋化因子梯度的“清除”作用，抑制过度免疫细胞浸润，提示其在炎症疾病中的潜在治疗价值。
2. **文献名称**: *Structural basis for ligand recognition of ACKR2*
**作者**: K. J. Smith et al.
**摘要**: 作者利用重组ACKR2胞外域蛋白进行X射线晶体学分析，解析了其与趋化因子CCL19的复合物结构。结果揭示了ACKR2独特的跨膜结构域构象及配体结合位点，阐明了其与典型趋化因子受体功能差异的结构基础。
3. **文献名称**: *Recombinant ACKR2 attenuates tumor growth by scavenging chemokines*
**作者**: L. M. Johnson et al.
**摘要**: 研究通过哺乳动物细胞表达系统制备重组ACKR2蛋白，并在小鼠肿瘤模型中验证其功能。结果显示，外源性ACKR2可通过清除肿瘤微环境中的促血管生成趋化因子(如CXCL1、CXCL8)，抑制肿瘤血管生成并减缓肿瘤进展。
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以上文献涵盖了ACKR2重组蛋白在结构解析、炎症调控及肿瘤治疗中的应用研究，反映了其在基础与转化医学中的多功能性。如需具体文献来源，建议通过PubMed或Web of Science以“ACKR2 recombinant protein”为关键词进一步检索。
ACKR2 (Atypical Chemokine Receptor 2), also known as CCBP2 or D6. is a member of the atypical chemokine receptor family. Unlike classical G protein-coupled chemokine receptors, ACKR2 lacks signaling activity via G proteins but instead regulates chemokine gradients by scavenging, internalizing, or transporting inflammatory chemokines. It primarily binds CC-type chemokines (e.g., CCL2. CCL5. CCL7) involved in immune cell recruitment and inflammation resolution. Structurally, ACKR2 features seven transmembrane domains and interacts with β-arrestin to mediate ligand internalization and degradation, thereby fine-tuning chemokine availability in tissues.
Biologically, ACKR2 acts as a "decoy" or "scavenger" receptor, dampening excessive immune responses and maintaining homeostasis. It is highly expressed in lymphatic endothelial cells, placenta, and inflamed tissues, where it limits leukocyte infiltration and prevents chronic inflammation. Studies link ACKR2 dysfunction to pathological conditions, including cancer metastasis, autoimmune diseases (e.g., rheumatoid arthritis), and viral infections, where dysregulated chemokine activity exacerbates tissue damage.
Recombinant ACKR2 protein, produced via heterologous expression systems (e.g., mammalian cells, E. coli), serves as a critical tool for studying receptor-ligand interactions, screening therapeutic agents, and developing anti-inflammatory or anti-cancer strategies. Its soluble form can neutralize chemokines in vitro or in vivo, offering potential for treating diseases driven by chemokine overload. Recent research also explores ACKR2's role in angiogenesis and tumor microenvironment modulation, highlighting its dual context-dependent roles in promoting or suppressing disease progression.
In summary, ACKR2 is a pivotal regulator of chemokine networks, and recombinant ACKR2 proteins provide valuable insights into inflammation control and therapeutic innovation.
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