| 纯度 | >85%SDS-PAGE. |
| 种属 | Human |
| 靶点 | FSTL3 |
| Uniprot No | O95633 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 27-263aa |
| 氨基酸序列 | MGSG NPAPGGVCWL QQGQEATCSL VLQTDVTRAE CCASGNIDTA WSNLTHPGNK INLLGFLGLV HCLPCKDSCD GVECGPGKAC RMLGGRPRCE CAPDCSGLPA RLQVCGSDGA TYRDECELRA ARCRGHPDLS VMYRGRCRKS CEHVVCPRPQ SCVVDQTGSA HCVVCRAAPC PVPSSPGQEL CGNNNVTYIS SCHMRQATCF LGRSIGVRHA GSCAGTPEEP PGGESAEEEE NFV |
| 预测分子量 | 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FSTL3重组蛋白的3篇代表性文献摘要(文献信息为模拟示例，仅供参考)：
1. **文献名称**：*FSTL3 as a critical regulator of glucose metabolism through TGF-β signaling*
**作者**：Smith A, et al.
**摘要**：研究利用重组人FSTL3蛋白体外处理肝细胞，发现其通过抑制TGF-β超家族成员(如activin)的活性，显著影响胰岛素敏感性相关基因表达，提示FSTL3在2型糖尿病病理机制中的作用。
2. **文献名称**：*Recombinant FSTL3 inhibits tumor growth by modulating immune cell infiltration*
**作者**：Chen L, et al.
**摘要**：在小鼠模型中注射大肠杆菌表达的重组FSTL3蛋白，观察到肿瘤微环境中调节性T细胞(Tregs)比例下降，CD8+ T细胞活性增强，表明FSTL3可能通过免疫调节发挥抗肿瘤作用。
3. **文献名称**：*Structural and functional characterization of FSTL3 protein produced in mammalian cells*
**作者**：Wang Y, et al.
**摘要**：利用HEK293细胞系统高效表达重组FSTL3蛋白，通过X射线晶体学解析其三维结构，揭示其与activin A结合的关键结构域，为开发针对FSTL3的靶向药物提供结构基础。
注：以上内容基于公开领域知识模拟生成，实际文献需通过PubMed/Google Scholar等平台检索确认。
Follistatin-like 3 (FSTL3), also known as follistatin-related gene (FLRG), is a secreted glycoprotein belonging to the follistatin family. It plays a critical role in regulating cellular processes by binding and modulating members of the transforming growth factor-beta (TGF-β) superfamily, particularly activins and myostatin. These interactions influence diverse physiological pathways, including muscle development, metabolism, immune response, and tissue fibrosis. FSTL3 is expressed in various tissues, such as skeletal muscle, liver, and placenta, and its dysregulation has been linked to metabolic disorders, cancer progression, and cardiovascular diseases.
Structurally, FSTL3 contains two follistatin-like domains and a Kazal-type protease inhibitor motif, enabling its high-affinity binding to target growth factors. Unlike follistatin, FSTL3 exhibits selective inhibition of activin and myostatin over bone morphogenetic proteins (BMPs), making it a key regulator of TGF-β signaling balance. This specificity underpins its involvement in conditions like insulin resistance, muscle atrophy, and fibrotic remodeling.
Recombinant FSTL3 protein is produced using engineered expression systems (e.g., mammalian cells or bacteria) to ensure proper folding and post-translational modifications. Its therapeutic and research applications are growing due to its potential as a biomarker or therapeutic agent. For instance, recombinant FSTL3 is used to study mechanisms of metabolic syndrome, muscle-wasting diseases, and fibrosis. Conversely, neutralizing FSTL3 activity has shown promise in preclinical models for enhancing muscle growth or mitigating fibrotic damage.
Despite progress, challenges remain in understanding its context-dependent roles and optimizing delivery strategies. Ongoing research focuses on clarifying its dual regulatory functions and exploring clinical applications in chronic diseases.
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