| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | TMEM110 |
| Uniprot No | Q86TL2 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-294 aa |
| 活性数据 | MQGPAGNASRGLPGGPPSTVASGAGRCESGALMHSFGIFLQGLLGVVAFSTLMLKRFREPKHERRPWRIWFLDTSKQAIGMLFIHFANVYLADLTEEDPCSLYLINFLLDATVGMLLIYVGVRAVSVLVEWQQWESLRFGEYGDPLQCGAWVGQCALYIVIMIFEKSVVFIVLLILQWKKVALLNPIENPDLKLAIVMLIVPFFVNALMFWVVDNFLMRKGKTKAKLEERGANQDSRNGSKVRYRRAASHEESESEILISADDEMEESDVEEDLRRLTPLKPVKKKKHRFGLPV |
| 分子量 | 59.6 kDa |
| 蛋白标签 | GST-tag at N-terminal |
| 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. |
以下是关于重组人TMEM110蛋白的参考文献示例(内容为假设性示例，供参考)：
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1. **文献名称**: *TMEM110 regulates ER-mitochondria contacts and cell survival*
**作者**: Giordano F. et al. (2020)
**摘要**: 研究揭示了TMEM110蛋白作为内质网(ER)和线粒体间膜接触点的关键调控因子，通过重组人TMEM110蛋白实验证实其与STIM1蛋白互作，参与钙稳态调控及细胞凋亡抵抗。
2. **文献名称**: *Structural insights into the function of human TMEM110 using cryo-EM*
**作者**: Chen L. et al. (2021)
**摘要**: 通过冷冻电镜解析了重组TMEM110蛋白的三维结构，发现其具有独特的跨膜螺旋构象，为理解其在细胞器膜相互作用中的分子机制提供了结构基础。
3. **文献名称**: *TMEM110 modulates viral replication by altering ER membrane dynamics*
**作者**: Alvarez J. et al. (2019)
**摘要**: 利用重组TMEM110蛋白过表达模型，证明该蛋白通过重塑内质网膜形态影响RNA病毒复制复合体的形成，提示其在先天免疫中的作用。
4. **文献名称**: *TMEM110 deficiency disrupts cardiac calcium handling in mice*
**作者**: Wang Y. et al. (2022)
**摘要**: 通过基因编辑及重组蛋白回补实验，发现TMEM110缺失导致心肌细胞线粒体-内质网钙信号异常，可能与心肌病相关。
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**注意**：以上文献为模拟示例，实际研究中请通过PubMed、Google Scholar等平台检索真实文献。TMEM110相关研究多集中于细胞器互作、钙信号或疾病机制领域。
Transmembrane protein 110 (TMEM110), also known as STIMATE, is a poorly characterized human protein encoded by the *TMEM110* gene. It is a multi-pass transmembrane protein localized primarily to the endoplasmic reticulum (ER) and ER-mitochondria contact sites. Structural predictions suggest it contains 4-6 transmembrane domains, though experimental validation of its topology remains limited.
TMEM110 gained attention for its role in regulating store-operated calcium entry (SOCE), a critical process in cellular calcium signaling. It directly interacts with stromal interaction molecule 1 (STIM1), a key calcium sensor in the ER, modulating STIM1 oligomerization and its interaction with Orai1 calcium channels. This interaction positions TMEM110 as a regulatory component of the cellular response to ER calcium depletion. Emerging studies link TMEM110 to the unfolded protein response (UPR), where it influences ER stress-mediated apoptosis through mechanisms involving calcium flux and ER-mitochondrial crosstalk.
Pathologically, TMEM110 overexpression has been observed in certain cancers, including lung adenocarcinoma, where it may promote tumor cell survival under hypoxic stress. Conversely, reduced TMEM110 expression correlates with worsened outcomes in myocardial ischemia-reperfusion injury models. Despite these associations, its precise molecular functions and disease relevance remain under investigation. Recent proteomic studies suggest potential roles in membrane trafficking and lipid metabolism, highlighting the need for deeper mechanistic exploration. Current research tools include knockout mouse models showing no overt developmental defects, suggesting functional redundancy or context-specific roles. Further studies are required to fully elucidate its biological significance and therapeutic potential.
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