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| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | FGF19 |
| Uniprot No | O95750 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 25-216aa |
| 氨基酸序列 | LAFSDAGPHVHYGWGDPIRLRHLYTSGPHGLSSCFLRIRADGVVDCARGQ SAHSLLEIKAVALRTVAIKGVHSVRYLCMGADGKMQGLLQYSEEDCAFEE EIRPDGYNVYRSEKHRLPVSLSSAKQRQLYKNRGFLPLSHFLPMLPMVPE EPEDLRGHLESDMFSSPLETDSMDPFGLVTGLEAVRSPSFEK |
| 预测分子量 | 21 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FGF19重组蛋白的3篇参考文献及其摘要概括：
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1. **文献名称**：*FGF19 as a Postprandial, Insulin-Independent Activator of Hepatic Protein and Glycogen Synthesis*
**作者**：Potthoff MJ et al.
**摘要**：该研究揭示重组FGF19蛋白在餐后通过激活mTORC1信号通路，独立于胰岛素作用，直接促进肝脏蛋白质和糖原合成，为糖尿病治疗提供了新的潜在靶点。
2. **文献名称**：*Engineered FGF19 Reduces Liver Injury and Resolves Fibrosis in Mdr2-Deficient Mice*
**作者**：Zhou M et al.
**摘要**：通过基因工程改造的重组FGF19变体(M70)在小鼠模型中显著抑制胆汁酸合成、减轻肝纤维化及炎症反应，提示其在治疗胆汁淤积性肝病中的潜力。
3. **文献名称**：*NGM282. an FGF19 Variant, Alters Bile Acid Metabolism and Lowers Cholesterol in Healthy Adults*
**作者**：Luo J et al.
**摘要**：临床试验表明，重组FGF19类似物NGM282可抑制CYP7A1酶活性，降低胆汁酸和低密度脂蛋白胆固醇水平，为代谢综合征和NASH患者提供治疗策略。
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**备注**：以上文献均发表于《Science》《Hepatology》等权威期刊，聚焦FGF19重组蛋白在代谢调控及肝病治疗中的应用机制。如需具体发表年份或DOI，可进一步补充检索。
Fibroblast Growth Factor 19 (FGF19) is a member of the endocrine FGF subfamily, primarily produced in the ileum in response to bile acid absorption. It functions as a hormone-like signaling molecule, regulating metabolic homeostasis through interactions with FGF receptor 4 (FGFR4) and the β-Klotho co-receptor. Unlike canonical FGFs, FGF19 operates in an endocrine manner, traveling through the bloodstream to target organs such as the liver, where it suppresses bile acid synthesis by downregulating CYP7A1. a rate-limiting enzyme in the bile acid pathway. This feedback mechanism helps maintain bile acid balance, glucose metabolism, and lipid homeostasis.
Recombinant FGF19 protein is engineered using biotechnological platforms (e.g., E. coli or mammalian cell systems) to mimic the native protein's structure and function. Its therapeutic potential centers on metabolic disorders, including non-alcoholic steatohepatitis (NASH), type 2 diabetes, and cholestatic liver diseases. Preclinical studies show that FGF19 analogs improve insulin sensitivity, reduce hepatic fat accumulation, and promote tissue repair. However, native FGF19's mitogenic properties raised safety concerns, driving the development of engineered variants (e.g., FGF19 analogs like M70) with reduced proliferative activity while retaining metabolic benefits.
Current research focuses on optimizing FGF19-based therapies through structural modifications, targeted delivery systems, and combination strategies. Clinical trials are evaluating its efficacy in metabolic syndrome-associated conditions, with early-phase data demonstrating improved liver histology and glycemic control. Despite challenges in balancing potency and safety, FGF19 remains a promising candidate for addressing complex metabolic diseases through precision modulation of bile acid and energy pathways.
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