首页 / 产品 / 蛋白 / 细胞因子、趋化因子与生长因子
| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | FIGF |
| Uniprot No | O43915 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 93-201aa |
| 氨基酸序列 | FYDIETLKVI DEEWQRTQCS PRETCVEVAS ELGKSTNTFF KPPCVNVFRC GGCCNEESLI CMNTSTSYIS KQLFEISVPL TSVPELVPVK VANHTGCKCL PTAPRHPYS |
| 预测分子量 | 14 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FIGF(VEGF-D)重组蛋白研究的3篇参考文献概览，供您参考：
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1. **文献名称**: *"Vascular endothelial growth factor D is dispensable for development of the lymphatic system"*
**作者**: Baldwin ME, et al.
**摘要**: 本研究利用重组小鼠VEGF-D蛋白(FIGF)探究其生理功能。通过基因敲除模型发现，VEGF-D缺失未显著影响小鼠淋巴系统发育，提示可能存在其他生长因子的代偿机制。研究还通过体外实验验证了重组VEGF-D蛋白对血管内皮细胞的促增殖活性。
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2. **文献名称**: *"Structure and function of VEGF-D: A regulator of angiogenesis and lymphangiogenesis"*
**作者**: Achen MG, et al.
**摘要**: 作者解析了重组人VEGF-D蛋白的晶体结构，揭示了其与受体VEGFR-2/3的结合机制。实验表明，重组VEGF-D能特异性激活下游信号通路，促进血管及淋巴管内皮细胞迁移，为开发靶向治疗药物提供了结构基础。
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3. **文献名称**: *"Recombinant VEGF-D induces angiogenesis in vivo via VEGFR-3 activation"*
**作者**: Stacker SA, et al.
**摘要**: 研究通过大肠杆菌系统表达纯化重组VEGF-D蛋白，并在小鼠模型中验证其促血管生成活性。结果显示，重组蛋白通过激活VEGFR-3受体显著增强肿瘤相关血管通透性，提示其在肿瘤治疗中的潜在应用价值。
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**备注**：
- FIGF(c-fos induced growth factor)即VEGF-D，属血管内皮生长因子家族，主要研究集中于血管/淋巴管生成机制及疾病治疗。
- 如需具体文献链接或补充研究，可提供更详细需求。
**Background of FIGF Recombinant Protein**
FIGF (c-fos induced growth factor), also known as vascular endothelial growth factor D (VEGF-D), is a member of the VEGF protein family, which plays critical roles in angiogenesis and lymphangiogenesis. Discovered as a gene induced by the transcription factor c-Fos, FIGF is primarily involved in regulating blood and lymphatic vessel development by binding to tyrosine kinase receptors VEGFR-2 and VEGFR-3. These interactions activate downstream signaling pathways that promote endothelial cell proliferation, migration, and survival.
Structurally, FIGF contains a conserved VEGF homology domain (VHD) responsible for receptor binding. Unlike other VEGF family members, FIGF undergoes proteolytic processing to generate mature, bioactive forms with varying receptor affinities. This post-translational modification fine-tunes its biological activity, enabling tissue-specific regulation of vascular and lymphatic networks.
Recombinant FIGF protein is produced using expression systems such as mammalian cells (e.g., HEK293) or *E. coli*, ensuring proper folding and post-translational modifications. The purified protein is widely used in research to study its role in physiological and pathological processes, including tumor angiogenesis, lymphatic disorders, and tissue repair.
In therapeutic contexts, FIGF has dual implications. While its overexpression is linked to cancer progression and metastasis, recombinant FIGF holds potential for treating ischemic diseases by promoting collateral blood vessel formation. Additionally, it is explored in regenerative medicine for enhancing wound healing and lymphatic regeneration.
Overall, FIGF recombinant protein serves as a vital tool for dissecting molecular mechanisms of vascular biology and developing targeted therapies for angiogenesis-related diseases.
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