| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | CDK5R1 |
| Uniprot No | Q15078 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 99-307aa |
| 氨基酸序列 | AQPPPAQPPAPPASQLSGSQTGGSSSVKKAPHPAVTSAGTPKRVIVQASTSELLRCLGEFLCRRCYRLKHLSPTDPVLWLRSVDRSLLLQGWQDQGFITPANVVFLYMLCRDVISSEVGSDHELQAVLLTCLYLSYSYMGNEISYPLKPFLVESCKEAFWDRCLSVINLMSSKMLQINADPHYFTQVFSDLKNESGQEDKKRLLLGLDR |
| 预测分子量 | 27.3 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CDK5R1(p35)重组蛋白的3篇代表性文献及其摘要概括：
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1. **标题**：*Conversion of p35 to p25 deregulates Cdk5 activity and promotes neurodegeneration*
**作者**：Patrick, G.N.等
**摘要**：该研究通过重组蛋白实验揭示了p35在神经元中被蛋白酶切割为p25的过程，证明p25异常积累会导致CDK5激酶活性持续激活，与阿尔茨海默病中tau蛋白过度磷酸化及神经退行性病变相关。
2. **标题**：*Structure of the monomeric mutant of Cdk5/p25*
**作者**：Tarricone, C.等
**摘要**：研究者利用重组CDK5和p25蛋白共表达系统，解析了CDK5/p25复合物的晶体结构，阐明了p25如何通过特异性结构域激活CDK5.为设计CDK5抑制剂提供了结构基础。
3. **标题**：*Regulation of the CDK5 activator protein p35 through proteasomal degradation*
**作者**：Sahlgren, C.M.等
**摘要**：本研究通过在大肠杆菌中表达重组p35蛋白，结合体外泛素化实验，揭示了p35的稳定性受泛素-蛋白酶体系统调控，并证明其降解异常可能影响神经发育和疾病进程。
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以上文献涉及重组CDK5R1(p35/p25)的表达、功能及结构研究，涵盖其在激酶激活机制、神经退行性疾病中的作用及调控途径。
CDK5R1. also known as p35. is a regulatory subunit of cyclin-dependent kinase 5 (CDK5), a serine/threonine kinase critical for neuronal development, synaptic plasticity, and cell cycle regulation. Unlike other cyclin-dependent kinases, CDK5 requires activation through binding to its regulatory partners, primarily CDK5R1 or its proteolytic product p25. CDK5R1 is expressed predominantly in the nervous system, where it forms a complex with CDK5 to regulate processes like axon guidance, dopamine signaling, and apoptosis. Dysregulation of the CDK5-p35/p25 pathway has been implicated in neurodegenerative disorders, including Alzheimer’s disease, where aberrant cleavage of p35 to p25 leads to hyperactivation of CDK5 and neuronal toxicity.
Recombinant CDK5R1 protein is produced using genetic engineering techniques, typically by expressing the gene in bacterial (e.g., *E. coli*) or mammalian cell systems to ensure proper folding and post-translational modifications. The recombinant protein retains the ability to bind and activate CDK5. making it a valuable tool for studying kinase activity, protein-protein interactions, and signaling mechanisms in vitro. Researchers use it to investigate CDK5’s role in neurodevelopment, neurodegeneration, and cancer, where CDK5 overexpression has been observed. Additionally, it serves as a substrate or target in drug discovery efforts aimed at modulating CDK5 activity for therapeutic purposes. Quality control assays, such as kinase activity tests and Western blotting, are employed to validate its functionality. The availability of recombinant CDK5R1 has accelerated mechanistic studies and high-throughput screening for potential inhibitors or stabilizers of the CDK5-p35 complex.
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