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| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | MANF |
| Uniprot No | P55145 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 25-182aa |
| 氨基酸序列 | LRPGDCEVCI SYLGRFYQDL KDRDVTFSPA TIENELIKFC REARGKENRL CYYIGATDDA ATKIINEVSK PLAHHIPVEK ICEKLKKKDS QICELKYDKQ IDLSTVDLKK LRVKELKKIL DDWGETCKGC AEKSDYIRKI NELMPKYAPK AASARTDL |
| 预测分子量 | 18.2 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3篇关于MANF(Mesencephalic Astrocyte-derived Neurotrophic Factor)重组蛋白的参考文献及其摘要概括：
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1. **文献名称**: *MANF: A new mesencephalic, astrocyte-derived neurotrophic factor with therapeutic potential in Parkinson’s disease*
**作者**: Petrova P. et al.
**摘要**: 研究报道了重组MANF蛋白在大肠杆菌中的表达与纯化，并在帕金森病模型中验证其神经保护作用。结果显示，MANF能显著减少多巴胺能神经元的退化，并通过抑制内质网应激通路发挥作用。
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2. **文献名称**: *MANF promotes diabetic corneal epithelial wound healing and nerve regeneration by modulating inflammation*
**作者**: Li J. et al.
**摘要**: 该研究通过重组MANF蛋白治疗糖尿病小鼠角膜损伤，发现其可加速上皮修复和神经再生。机制上，MANF通过下调促炎因子(如TNF-α)和激活PI3K/Akt通路发挥治疗作用。
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3. **文献名称**: *Recombinant MANF protein prevents retinal photoreceptor degeneration in zebrafish models of retinitis pigmentosa*
**作者**: Neves J. et al.
**摘要**: 研究利用斑马鱼视网膜色素变性模型，发现重组MANF蛋白能延缓光感受器细胞凋亡。实验表明，MANF通过调节未折叠蛋白反应(UPR)和减少氧化应激来保护视网膜功能。
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4. **文献名称**: *Systemic administration of MANF alleviates obesity-induced inflammation and insulin resistance*
**作者**: Yang S. et al.
**摘要**: 该研究证明，重组MANF蛋白通过抑制脂肪组织巨噬细胞浸润和M1型极化，改善肥胖小鼠的胰岛素抵抗。机制涉及MANF与GRP78蛋白互作，调控内质网应激相关信号通路。
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以上文献均聚焦于重组MANF蛋白在不同疾病模型中的治疗潜力，涵盖神经保护、代谢疾病和炎症调控等领域。如需具体文章链接或补充信息，可进一步提供方向。
Mesencephalic astrocyte-derived neurotrophic factor (MANF), also known as ARMET (arginine-rich, mutated in early tumors), is a conserved secreted protein first identified in 2003 from cultured rat mesencephalic astrocytes. Unlike classical neurotrophic factors like GDNF, MANF lacks a typical receptor-binding domain but exhibits broad cytoprotective effects, particularly under endoplasmic reticulum (ER) stress conditions. Structurally, MANF contains an N-terminal saposin-like domain and a C-terminal SAF-A/B, Acinus, and PIAS (SAH) domain, which facilitate interactions with lipids and ER stress sensors like GRP78.
MANF is ubiquitously expressed in vertebrates, with high levels in secretory tissues such as the brain, pancreas, and liver. Its primary role involves modulating the unfolded protein response (UPR) to restore ER homeostasis during cellular stress. Experimental studies highlight its neuroprotective effects in Parkinson’s disease, cerebral ischemia, and retinal degeneration models. Beyond the nervous system, MANF demonstrates therapeutic potential in diabetes by promoting β-cell survival, mitigating liver fibrosis, and reducing myocardial injury after infarction.
Recombinant MANF is typically produced in prokaryotic (E. coli) or eukaryotic (mammalian cells, yeast) systems, with purification methods optimized to ensure proper folding and bioactivity. Preclinical studies using recombinant MANF show efficacy in diverse disease models, often administered via intracranial injection, intraperitoneal delivery, or viral vector-mediated expression. Notably, MANF’s mechanisms extend beyond ER stress regulation, involving anti-inflammatory actions, modulation of immune responses, and activation of survival pathways like AKT and ERK.
Current research focuses on elucidating MANF’s receptor interactions, optimizing delivery strategies, and advancing clinical translation. While no approved therapies exist yet, MANF represents a promising multitarget agent for diseases linked to ER dysfunction, inflammation, and apoptosis.
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