| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | FAM13A1 |
| Uniprot No | O94988 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-202aa |
| 氨基酸序列 | MGAGALAICQSKAAVRLKEDMKKIVAVPLNEQKDFTYQKLFGVSLQELERQGLTENGIPAVVWNIVEYLTQHGLTQEGLFRVNGNVKVVEQLRLKFESGVPVELGKDGDVCSAASLLKLFLRELPDSLITSALQPRFIQLFQDGRNDVQESSLRDLIKELPDTHYCLLKYLCQFLTKVAKHHVQNRMNVHNLATVFGPNCFQ |
| 分子量 | 49.1 kDa |
| 蛋白标签 | GST-tag at N-terminal |
| 缓冲液 | 0 |
| 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. |
以下为关于重组人FAM13A1蛋白的文献示例(注：以下内容基于研究领域知识模拟，建议通过学术数据库核实具体文献)：
1. **"FAM13A1 Modulates Wnt/β-Catenin Signaling in Chronic Obstructive Pulmonary Disease"**
*作者：Kim et al. (2019)*
摘要：研究显示，重组人FAM13A1蛋白通过稳定β-catenin蛋白调控Wnt信号通路，可能影响慢性阻塞性肺疾病(COPD)的气道炎症和修复过程。实验使用体外表达的重组蛋白验证其与PP2A磷酸酶的相互作用。
2. **"Recombinant FAM13A1 Suppresses Lung Cancer Metastasis via Inhibition of EMT Pathways"**
*作者：Zhang et al. (2020)*
摘要：研究证明重组FAM13A1蛋白可抑制肺癌细胞的上皮-间质转化(EMT)，降低迁移和侵袭能力。机制分析表明其通过结合Smad3蛋白阻断TGF-β信号传导。
3. **"Structural Characterization of Human FAM13A1 and Its Interaction with Lipid Metabolites"**
*作者：Smith et al. (2021)*
摘要：通过X射线晶体学解析重组FAM13A1的蛋白结构，揭示其N端结构域与脂质代谢产物(如花生四烯酸)的结合能力，提示其在脂质代谢相关疾病中的潜在作用。
4. **"FAM13A1 Attenuates Oxidative Stress in Alveolar Epithelial Cells via Nrf2 Activation"**
*作者：Chen et al. (2022)*
摘要：体外实验表明，重组FAM13A1蛋白通过激活Nrf2通路增强肺泡细胞的抗氧化能力，可能为肺纤维化或COPD的治疗提供新靶点。
建议使用PubMed、Web of Science等数据库，以“recombinant FAM13A1”、“FAM13A1 protein function”等关键词检索最新文献。
**Background of Recombinant Human FAM13A1 Protein**
FAM13A1 (Family with sequence similarity 13 member A1) is a protein-coding gene implicated in diverse cellular processes, including cell signaling, metabolic regulation, and stress response. Initially identified through genome-wide association studies (GWAS), FAM13A1 has been linked to chronic obstructive pulmonary disease (COPD), lung cancer, and metabolic syndromes, suggesting its role in disease pathogenesis. Structurally, the human FAM13A1 protein contains conserved domains such as a coiled-coil domain, a Rho-GAP-like domain, and a highly variable intrinsically disordered region, which may facilitate protein-protein interactions and regulatory functions.
Recombinant FAM13A1 protein is engineered to enable functional studies, particularly to dissect its involvement in pathways like Wnt/β-catenin signaling, hypoxia-inducible factor (HIF) regulation, and lipid metabolism. For instance, FAM13A1 modulates β-catenin stability, influencing lung fibrosis and epithelial-mesenchymal transition. It also interacts with HIF-1α under hypoxic conditions, affecting cellular adaptation to low oxygen.
Produced via expression systems like *E. coli* or mammalian cells, recombinant FAM13A1 is purified for *in vitro* assays, antibody development, and mechanistic studies. Recent findings highlight its epigenetic regulatory roles, including phosphorylation-dependent interactions and ubiquitination-mediated degradation. Despite progress, its precise molecular mechanisms remain under investigation, making recombinant FAM13A1 a critical tool for exploring its therapeutic potential in pulmonary, metabolic, and oncological disorders.
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