| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | CDK5 |
| Uniprot No | Q00535 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-292aa |
| 氨基酸序列 | MQKYEKLEKIGEGTYGTVFKAKNRETHEIVALKRVRLDDDDEGVPSSALREICLLKELKHKNIVRLHDVLHSDKKLTLVFEFCDQDLKKYFDSCNGDLDPEIVKSFLFQLLKGLGFCHSRNVLHRDLKPQNLLINRNGELKLADFGLARAFGIPVRCYSAEVVTLWYRPPDVLFGAKLYSTSIDMWSAGCIFAELANAGRPLFPGNDVDDQLKRIFRLLGTPTEEQWPSMTKLPDYKPYPMYPATTSLVNVVPKLNATGRDLLQNLLKCNPVQRISAEEALQHPYFSDFCPP |
| 预测分子量 | 33.4 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CDK5重组蛋白的3篇代表性文献摘要：
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1. **《A critical role for CDK5 in regulating neuronal cell cycle and apoptosis》**
- **作者**: Dhavan R., Tsai L.H.
- **摘要**: 研究利用重组CDK5/p35蛋白，揭示了CDK5在调控神经元细胞周期退出和抑制凋亡中的关键作用，通过体外激酶实验证明其磷酸化底物特异性。
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2. **《Production of active human CDK5/p25 kinase complex in E. coli》**
- **作者**: Lew J., Winkfein R.J.
- **摘要**: 描述在大肠杆菌中高效表达并纯化具有激酶活性的人源CDK5/p25重组复合物，验证其通过磷酸化组蛋白H1的体外功能。
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3. **《CDK5-mediated phosphorylation of tau protein in Alzheimer’s disease pathology》**
- **作者**: Patrick G.N. et al.
- **摘要**: 通过重组CDK5与p25共表达，证实其在阿尔茨海默病模型中异常磷酸化tau蛋白，导致神经纤维缠结形成的分子机制。
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以上文献涵盖CDK5重组蛋白的制备、功能分析及其在疾病模型中的应用，均为该领域经典研究。如需扩展，可进一步检索近年涉及CRISPR/Cas9或类器官模型的CDK5研究。
**Background of CDK5 Recombinant Protein**
Cyclin-dependent kinase 5 (CDK5) is a serine/threonine kinase belonging to the CDK family but distinct in its regulation and function. Unlike other CDKs involved in cell cycle control, CDK5 is primarily active in postmitotic neurons, playing critical roles in neuronal development, synaptic plasticity, and neurotransmission. Its activity depends on association with non-cyclin activators, notably p35 or p39. which confer substrate specificity and subcellular localization. Dysregulation of CDK5. often linked to proteolytic cleavage of p35 into p25 (a hyperactive fragment), is implicated in neurodegenerative diseases like Alzheimer’s, Parkinson’s, and neuropsychiatric disorders, as well as cancer metastasis.
Recombinant CDK5 protein is produced via heterologous expression systems (e.g., *E. coli*, insect, or mammalian cells*) to study its biochemical properties, signaling mechanisms, and interactions. Purified CDK5 enables *in vitro* kinase assays, structural studies (e.g., X-ray crystallography), and drug screening for inhibitors targeting pathological CDK5-p25 activity. Its recombinant form often includes tags (e.g., GST, His) for affinity purification and detection. Research using CDK5 recombinant protein has advanced understanding of its role in tau phosphorylation (linked to neurofibrillary tangles), dopamine signaling, and cytoskeletal dynamics. Additionally, it serves as a tool to explore crosstalk with pathways like Wnt or PI3K/AKT, offering insights into therapeutic strategies for neurodegeneration and cancer. Challenges remain in mimicking native activation *in vitro* due to the necessity of co-expressing regulatory partners, underscoring the complexity of CDK5 biology.
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