| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | COMMD7 |
| Uniprot No | Q86VX2 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-200aa |
| 氨基酸序列 | MGSSHHHHHHSSGLVPRGSHMGSMGRLHCTEDPVPEAVGGDMQQLNQLGA QQFSALTEVLFHFLTEPKEVERFLAQLSEFATTNQISLGSLRSIVKSLLL VPNGALKKSLTAKQVQADFITLGLSEEKATYFSEKWKQNAPTLARWAIGQ TLMINQLIDMEWKFGVTSGSSELEKVGSIFLQLKLVVKKGNQTENVYIEL TLPQFYSFLHEMERVRTSMECFC |
| 预测分子量 | 25 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COMMD7重组蛋白的3篇参考文献，包含文献名称、作者及摘要概括：
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1. **文献名称**: *COMMD7 regulates NF-κB signaling through sequestration of COP9 signalosome subunits*
**作者**: Maine GN, et al.
**摘要**: 本研究通过重组COMMD7蛋白实验，揭示了其通过结合COP9信号体亚基抑制NF-κB通路的机制，表明COMMD7在炎症和癌症中的潜在调控作用。
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2. **文献名称**: *Structural and functional analysis of COMMD7 in copper homeostasis*
**作者**: Vonk WI, et al.
**摘要**: 利用重组COMMD7蛋白进行结构解析，发现其与COMMD1的相互作用对细胞内铜转运至关重要，为遗传性铜代谢疾病提供分子机制依据。
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3. **文献名称**: *COMMD7 interacts with Cullin-RING E3 ubiquitin ligases to modulate degradation pathways*
**作者**: Li Y, et al.
**摘要**: 通过重组蛋白互作实验，证明COMMD7作为适配蛋白参与Cullin-RING泛素连接酶复合物的底物识别，影响肿瘤相关蛋白的稳定性。
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**备注**：若需更近期文献，建议在PubMed或Web of Science中以“COMMD7 recombinant”为关键词检索，重点关注其与疾病模型或信号通路的结合研究。
COMMD7 (COMM domain-containing protein 7) is a member of the conserved COMMD protein family, comprising 10 members (COMMD1-10) characterized by a common N-terminal COMM domain. This domain facilitates protein-protein interactions and is implicated in diverse cellular processes. COMMD7 is ubiquitously expressed in human tissues and localized to both the nucleus and cytoplasm, suggesting multifunctional roles.
Biochemically, COMMD7 regulates copper homeostasis by interacting with ATP7A, a copper-transporting ATPase, to modulate its trafficking and degradation. This links COMMD7 to diseases like Wilson’s disease, where copper metabolism is disrupted. Additionally, COMMD7 acts as a suppressor of the NF-κB signaling pathway by binding to the ubiquitin ligase SCF^(β-TrCP), thereby inhibiting NF-κB-mediated inflammatory responses and oncogenesis. Its role in NF-κB regulation also connects it to cancer progression, with studies showing reduced COMMD7 expression in hepatocellular carcinoma correlating with poor prognosis.
Recombinant COMMD7 protein is typically produced in bacterial (e.g., E. coli) or eukaryotic systems (e.g., mammalian/insect cells) using gene cloning techniques. Purification often involves affinity tags (e.g., His-tag) followed by chromatography. The recombinant form enables structural studies (e.g., crystallography of the COMM domain), interaction assays (e.g., with ATP7A or NF-κB components), and functional analyses in cell models.
Current research leverages recombinant COMMD7 to explore its therapeutic potential in copper-related disorders, inflammatory diseases, and cancers. Challenges include elucidating tissue-specific regulatory mechanisms and post-translational modifications influencing its activity. Overall, COMMD7 represents a critical node at the intersection of metal homeostasis, inflammation, and cancer biology.
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