| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | TMEM59 |
| Uniprot No | Q9BXS4 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 37-323aa |
| 氨基酸序列 | AFDSVLGDTASCHRACQLTYPLHTYPKEEELYACQRGCRLFSICQFVDDG IDLNRTKLECESACTEAYSQSDEQYACHLGCQNQLPFAELRQEQLMSLMP KMHLLFPLTLVRSFWSDMMDSAQSFITSSWTFYLQADDGKIVIFQSKPEI QYAPHLEQEPTNLRESSLSKMSYLQMRNSQAHRNFLEDGESDGFLRCLSL NSGWILTTTLVLSVMVLLWICCATVATAVEQYVPSEKLSIYGDLEFMNEQ KLNRYPASSLVVVRSKTEDHEEAGPLPTKVNLAHSEI |
| 预测分子量 | 36 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TMEM59重组蛋白的3篇文献摘要信息(注：以下内容基于公开研究整理，部分为示例性描述)：
1. **文献名称**: "TMEM59 interacts with TREM2 and modulates its cleavage and phagocytic function in microglia"
**作者**: Zhang Y, et al.
**摘要**: 研究揭示了TMEM59重组蛋白与小胶质细胞中TREM2的相互作用，证明TMEM59通过调控TREM2的蛋白水解过程影响其吞噬功能，可能与阿尔茨海默病的病理机制相关。
2. **文献名称**: "TMEM59 deficiency disrupts autophagosome-lysosome fusion and exacerbates neuronal vulnerability in Parkinson's disease models"
**作者**: Li X, et al.
**摘要**: 通过构建TMEM59重组蛋白表达体系，发现TMEM59缺失导致自噬体-溶酶体融合障碍，加剧帕金森病模型中神经元的退行性病变，提示其参与神经保护机制。
3. **文献名称**: "Structural characterization of TMEM59 as a novel regulator of Wnt signaling pathway"
**作者**: Chen H, et al.
**摘要**: 利用重组TMEM59蛋白进行结构解析，发现其通过调控Wnt/β-catenin信号通路影响细胞增殖和分化，为癌症靶向治疗提供潜在分子靶点。
注：以上文献为示例，实际文献需通过PubMed或Web of Science检索确认。建议使用关键词“TMEM59 recombinant protein”或“TMEM59 function”查找最新实验研究。
**Background of TMEM59 Recombinant Protein**
TMEM59 (Transmembrane Protein 59), also known as LAPTM4B, is a conserved eukaryotic protein localized primarily in the Golgi apparatus and endosomal compartments. It features a four-transmembrane domain structure and plays roles in membrane trafficking, autophagy, and immune regulation. Studies link TMEM59 to neurodegenerative diseases, such as Alzheimer’s disease (AD), where it modulates amyloid precursor protein (APP) processing and β-amyloid production. Additionally, TMEM59 interacts with Toll-like receptors (TLRs) to regulate inflammatory responses, suggesting involvement in innate immunity.
The recombinant TMEM59 protein, produced via heterologous expression systems (e.g., *E. coli* or mammalian cells), retains functional domains for biochemical and cellular studies. Its recombinant form enables researchers to explore molecular mechanisms, such as its role in autophagy-lysosomal pathways or its impact on APP metabolism in AD models. Furthermore, TMEM59 overexpression or knockdown studies using recombinant variants have highlighted its dual role in promoting or inhibiting cancer progression, depending on cellular context, implicating it as a potential therapeutic target.
Current research leverages TMEM59 recombinant protein to decipher its structural motifs, post-translational modifications, and interactions with signaling molecules. These efforts aim to clarify its physiological relevance in health and disease, particularly in neuroinflammation, cancer biology, and lysosomal disorders. The protein’s multifunctionality underscores its importance as a research tool for uncovering novel pathways in membrane biology and disease pathogenesis.
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