| 纯度 | >95%SDS-PAGE. |
| 种属 | Human |
| 靶点 | GSKIP |
| Uniprot No | Q9P0R6 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-139aa |
| 氨基酸序列 | MGSSHHHHHHSSGLVPRGSHMETDCNPMELSSMSGFEEGSELNGFEGTDM KDMRLEAEAVVNDVLFAVNNMFVSKSLRCADDVAYINVETKERNRYCLEL TEAGLKVVGYAFDQVDDHLQTPYHETVYSLLDTLSPAYREAFGNALLQRL EALKRDGQS |
| 预测分子量 | 18 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GSKIP重组蛋白的3篇参考文献示例(注：文献名称及作者为模拟示例，供参考)：
---
1. **文献名称**：*GSKIP regulates Wnt/β-catenin signaling through interaction with GSK3β and Dishevelled*
**作者**：Chen L, et al.
**摘要**：本研究揭示了GSKIP重组蛋白在Wnt信号通路中的调控作用，证实其通过与GSK3β和Dishevelled蛋白的相互作用，抑制β-catenin的磷酸化降解，从而促进下游靶基因激活。实验采用重组人源GSKIP蛋白验证其分子结合能力。
---
2. **文献名称**：*Expression and purification of recombinant GSKIP in E. coli for structural analysis*
**作者**：Wang Y, et al.
**摘要**：报道了一种高效表达和纯化GSKIP重组蛋白的大肠杆菌系统，通过优化诱导条件及亲和层析技术获得高纯度蛋白。圆二色谱分析表明重组GSKIP具有稳定的α-螺旋结构，为后续功能研究奠定基础。
---
3. **文献名称**：*GSKIP-mediated mitochondrial dysfunction in neurodegenerative disease models*
**作者**：Kim S, et al.
**摘要**：研究发现，过表达重组GSKIP蛋白可加剧线粒体膜电位丧失和活性氧积累，提示其在阿尔茨海默病模型中可能通过干扰GSK3β的定位加剧神经元损伤。研究为神经退行性疾病的机制提供了新视角。
---
如需实际文献，建议通过PubMed或Google Scholar检索关键词“GSKIP recombinant protein”“GSK3β interaction protein”获取最新研究。
**Background of GSKIP Recombinant Protein**
GSKIP (GSK3β Interaction Protein) is a conserved eukaryotic protein known for its regulatory role in cellular signaling pathways, particularly those involving Glycogen Synthase Kinase 3 beta (GSK3β). Initially identified as a binding partner of GSK3β, GSKIP modulates the kinase’s activity, which is critical in processes such as glycogen metabolism, Wnt/β-catenin signaling, and cell cycle regulation. Structurally, GSKIP contains a conserved N-terminal domain that facilitates interaction with GSK3β and a C-terminal domain implicated in binding other signaling molecules, including components of the mitochondrial electron transport chain.
Recombinant GSKIP proteins are engineered using expression systems (e.g., *E. coli* or mammalian cells*) to produce purified, functional forms of the protein for research and therapeutic applications. These recombinant variants often include tags (e.g., His-tag, GST-tag) for efficient purification and detection. Studies highlight GSKIP’s dual role as both a scaffold and a regulatory protein. For instance, it acts as a negative regulator of GSK3β in the Wnt pathway by sequestering the kinase, thereby influencing β-catenin stability and transcriptional activity. Conversely, GSKIP promotes mitochondrial function by interacting with complex II (succinate dehydrogenase), linking cellular signaling to energy metabolism.
Dysregulation of GSKIP has been associated with diseases such as cancer, neurodegenerative disorders, and diabetes. For example, reduced GSKIP expression correlates with aberrant GSK3β activity in certain cancers, affecting cell proliferation and apoptosis. Recombinant GSKIP is widely used in mechanistic studies to dissect its interactions, post-translational modifications, and therapeutic potential. Recent advances also explore its utility in drug screening platforms targeting GSK3β-related pathologies. Overall, GSKIP recombinant proteins serve as vital tools for understanding cellular signaling networks and developing targeted therapies.
×
