首页 / 产品 / 蛋白 / 细胞因子、趋化因子与生长因子
| 纯度 | >95%SDS-PAGE. |
| 种属 | Human |
| 靶点 | GDF15 |
| Uniprot No | Q99988 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 197-308aa |
| 氨基酸序列 | ARNGDHCPLGPGRCCRLHTVRASLEDLGWADWVLSPREVQVTMCIGACPS QFRAANMHAQIKTSLHRLKPDTVPAPCCVPASYNPMVLIQKTDTGVSLQT YDDLLAKDCHCI |
| 预测分子量 | 12 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GDF15重组蛋白的代表性文献摘要概括：
---
1. **文献名称**: *GDF15 mediates the effects of metformin on body weight and energy balance*
**作者**: Coll AP et al.
**摘要**: 该研究揭示二甲双胍通过上调GDF15表达，促进重组GDF15蛋白分泌，从而抑制食欲并减轻肥胖小鼠体重，首次将GDF15与经典降糖药物的代谢调控机制相关联。(Nature 2020)
---
2. **文献名称**: *Non-homeostatic body weight regulation through a brainstem-restricted receptor for GDF15*
**作者**: Hsu JY et al.
**摘要**: 发现GFRAL为GDF15的专属受体，位于脑干孤束核。重组GDF15蛋白通过激活GFRAL-介导的信号通路，抑制摄食行为并调节能量代谢，为肥胖治疗提供新靶点。(Nature 2017)
---
3. **文献名称**: *TGF-β superfamily cytokine MIC-1/GDF15 in cancer cachexia*
**作者**: Johnen H et al.
**摘要**: 证实肿瘤源性GDF15重组蛋白通过中枢神经系统引发肌肉萎缩和脂肪分解，直接导致癌症恶病质，阻断GDF15可逆转小鼠模型中的恶病质表型。(Cancer Research 2007)
---
4. **文献名称**: *GDF15 promotes weight loss by enhancing energy expenditure in muscle*
**作者**: Emmerson PJ et al.
**摘要**: 发现重组GDF15蛋白不仅抑制食欲，还能直接增加骨骼肌线粒体氧化代谢，促进脂肪燃烧，双重机制协同降低体脂。(Cell Metabolism 2018)
---
这些研究从分子机制到疾病治疗，系统阐述了GDF15重组蛋白在代谢调控中的核心作用。
**Background of GDF15 Recombinant Protein**
Growth Differentiation Factor 15 (GDF15), a member of the transforming growth factor-beta (TGF-β) superfamily, is a stress-responsive cytokine implicated in diverse physiological and pathological processes. Initially identified as macrophage inhibitory cytokine-1 (MIC-1), GDF15 is secreted as a disulfide-linked homodimer and signals through a receptor complex involving GDNF-family receptor α-like (GFRAL) and RET tyrosine kinase, primarily in the brainstem. Its expression is low under normal conditions but rises dramatically during tissue injury, inflammation, mitochondrial dysfunction, and metabolic stress.
Recombinant GDF15 protein, produced via genetic engineering in systems like *E. coli* or mammalian cells, retains the biological activity of native GDF15. Research highlights its role in regulating appetite, energy homeostasis, and body weight by activating hindbrain neurons, making it a potential therapeutic target for obesity and metabolic disorders. Preclinical studies demonstrate that exogenous GDF15 reduces food intake, improves glucose tolerance, and mitigates insulin resistance.
Beyond metabolism, GDF15 is linked to cancer cachexia, cardiovascular diseases, and aging. Elevated serum GDF15 correlates with cancer progression and poor prognosis, partly due to its role in promoting muscle wasting and anorexia. Conversely, its cardioprotective effects in ischemia-reperfusion injury and heart failure are under investigation.
Despite therapeutic promise, challenges remain, including understanding tissue-specific signaling and managing side effects like muscle loss. Recent clinical trials exploring GDF15 analogs for obesity have shown efficacy but also underscored the need for balanced modulation. Overall, GDF15 recombinant protein represents a multifaceted tool for studying metabolic regulation and disease mechanisms, with translational potential awaiting further optimization.
×
