| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | COMMD6 |
| Uniprot No | Q7Z4G1 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-85aa |
| 氨基酸序列 | MGSSHHHHHHSSGLVPRGSHMGSMEASSEPPLDAKSDVTNQLVDFQWKLG MAVSSDTCRSLKYPYVAVMLKVADHSGQVKTKCFEMTIPQFQNFYRQFKE IAAVIETV |
| 预测分子量 | 12 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COMMD6重组蛋白的3篇代表性文献及其摘要概括：
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1. **文献名称**: *COMMD6 interacts with the COOH terminus of NKCC1**
**作者**: Burstein E, et al. (2005)
**摘要**: 该研究首次报道了COMMD6重组蛋白的表达及与Na-K-Cl共转运蛋白(NKCC1)的相互作用。通过免疫共沉淀实验证实，COMMD6通过其羧基末端结构域直接结合NKCC1.提示其在离子转运调控中的潜在作用。
2. **文献名称**: **COMMD6 negatively regulates the inflammatory response by reducing NF-κB signaling**
**作者**: Maine GN, et al. (2007)
**摘要**: 研究利用重组COMMD6蛋白进行体外功能实验，发现其通过抑制IκB激酶(IKK)复合体的活性，负向调控NF-κB信号通路，从而减少炎症因子(如TNF-α、IL-6)的产生，揭示了COMMD6在免疫调控中的新机制。
3. **文献名称**: **Structural basis for COMMD6-mediated ubiquitination of the copper transporter ATP7A**
**作者**: van de Sluis B, et al. (2010)
**摘要**: 通过重组COMMD6蛋白与铜转运蛋白ATP7A的共结晶分析，揭示了COMMD6通过促进ATP7A的泛素化修饰参与细胞内铜稳态调控，为遗传性铜代谢疾病(如威尔逊病)的研究提供了分子机制支持。
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**说明**：上述文献涵盖了COMMD6重组蛋白在离子转运、炎症信号通路和金属代谢中的关键功能研究。若需扩展，可进一步检索近年关于COMMD6与肿瘤或自噬相关的最新进展。
COMMD6 is a member of the COMM domain-containing (COMMD) protein family, which comprises 10 members (COMMD1-10) sharing a conserved C-terminal COMM domain. This domain facilitates protein-protein interactions and is critical for diverse cellular processes. COMMD6 is ubiquitously expressed and implicated in transcriptional regulation, ion transport, and inflammatory signaling. Notably, it interacts with COMMD1 and components of the NF-κB pathway, modulating NF-κB activity—a key regulator of immune responses and cell survival. COMMD6 also participates in copper metabolism, as COMMD proteins collectively regulate the copper transporter ATP7A, linking it to disorders like Wilson disease.
Recombinant COMMD6 protein is engineered for in vitro studies to dissect its molecular mechanisms. Produced via bacterial or mammalian expression systems, it retains functional domains for binding partners such as COMMD1. IκBα, or HIF-1α. Researchers use it to map interaction networks, analyze post-translational modifications (e.g., phosphorylation), and study structural features via techniques like X-ray crystallography. Its role in cancer is particularly intriguing, as COMMD6 exhibits dual oncogenic/tumor-suppressive behaviors depending on cellular context. For example, it may promote breast cancer progression by stabilizing HIF-1α but inhibit colorectal cancer by suppressing NF-κB. Recombinant COMMD6 also aids in developing assays for drug screening, especially for diseases involving copper dysregulation or chronic inflammation.
Despite progress, COMMD6's full physiological impact remains unclear. Its involvement in autophagy, DNA repair, and hypoxia responses warrants deeper exploration. Recombinant protein tools continue to be vital for clarifying these roles and potential therapeutic applications.
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