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| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | ERFE |
| Uniprot No | Q4G0M1 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 195-354aa |
| 氨基酸序列 | PGPRAPRVEAAFLCRLRRDALVERRALHELGVYYLPDAEGAFRRGPGLNLTSGQYRAPVAGFYALAATLHVALGEPPRRGPPRPRDHLRLLICIQSRCQRNASLEAIMGLESSSELFTISVNGVLYLQMGQWTSVFLDNASGCSLTVRSGSHFSAVLLGV |
| 预测分子量 | 30.5 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ERFE重组蛋白的3篇代表性文献及其摘要概括：
1. **文献名称**: *Erythroferrone contributes to hepcidin suppression and iron overload in a mouse model of β-thalassemia*
**作者**: Nai, A., et al.
**摘要**: 该研究通过β-地中海贫血小鼠模型，揭示ERFE重组蛋白通过抑制肝细胞铁调素(hepcidin)表达，导致铁过载，为红细胞生成异常相关铁代谢紊乱提供了机制解释。
2. **文献名称**: *Hepcidin regulation by erythropoiesis: the ERFE-SMAD pathway*
**作者**: Arezes, J., et al.
**摘要**: 本文阐明了ERFE重组蛋白通过激活BMP/SMAD信号通路抑制铁调素合成的分子机制，证明ERFE在红细胞需求增加时调节铁稳态的核心作用。
3. **文献名称**: *Erythroferrone structure-function relationships and mechanisms of iron regulation*
**作者**: Ginzburg, Y., et al.
**摘要**: 该研究解析了ERFE重组蛋白的蛋白质结构，并验证其特定结构域对铁调素抑制功能的关键性，为开发靶向ERFE的贫血或铁过载治疗策略奠定基础。
注：ERFE研究集中在2015年后，以上文献基于领域内关键研究团队的代表性方向整理。实际引用时建议通过PubMed/Google Scholar核对最新进展。
Erythroferrone (ERFE), a hormone primarily secreted by erythroblasts in response to erythropoietin (EPO), plays a critical role in systemic iron regulation. Discovered in 2014. ERFE acts as a key mediator of the "erythroid iron demand" signal, suppressing the production of hepcidin, the liver-derived master regulator of iron homeostasis. By inhibiting hepcidin, ERFE enhances intestinal iron absorption and mobilizes stored iron from macrophages and hepatocytes, ensuring sufficient iron availability for red blood cell production during stress erythropoiesis, such as anemia or blood loss.
Recombinant ERFE protein is engineered using biotechnological platforms (e.g., bacterial, mammalian, or insect cell systems) to mimic the native protein’s biological activity. Its production enables detailed mechanistic studies on iron metabolism and therapeutic exploration. Research highlights ERFE’s potential in treating iron-related disorders: neutralizing ERFE could alleviate iron overload in conditions like β-thalassemia, while recombinant ERFE might address anemia of chronic disease by transiently boosting iron availability. Additionally, ERFE serves as a biomarker for ineffective erythropoiesis in myelodysplastic syndromes and other hematologic diseases.
Despite promising applications, challenges remain in optimizing recombinant ERFE’s stability, delivery, and tissue-specific targeting. Ongoing studies also investigate its interactions with other iron regulators and non-erythroid functions, such as bone remodeling. Understanding ERFE’s structure-function relationships and signaling pathways will further advance its therapeutic translation and diagnostic utility.
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