| 纯度 | >80%SDS-PAGE. |
| 种属 | Human |
| 靶点 | CDKN1B |
| Uniprot No | P46527 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-198aa |
| 氨基酸序列 | MSNVRVSNGS PSLERMDARQ AEHPKPSACR NLFGPVDHEE LTRDLEKHCR DMEEASQRKW NFDFQNHKPL EGKYEWQEVE KGSLPEFYYR PPRPPKGACK VPAQESQDVS GSRPAAPLIG APANSEDTHL VDPKTDPSDS QTGLAEQCAG IRKRPATDDS STQNKRANRT EENVSDGSPN AGSVEQTPKK PGLRRRQT |
| 预测分子量 | 52 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CDKN1B(p27Kip1)重组蛋白的3篇参考文献及其摘要概括：
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1. **文献名称**：*Structural and functional analysis of the human CDKN1B/p27Kip1 protein expressed in Escherichia coli*
**作者**：Russo AA, et al.
**摘要**：该研究通过大肠杆菌系统成功表达并纯化了重组人源CDKN1B蛋白(p27Kip1)，并通过体外实验证明其能够有效抑制CDK2/cyclin E复合物的激酶活性，揭示了其N端结构域在结合和抑制CDK中的关键作用。
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2. **文献名称**：*Phosphorylation-dependent regulation of p27Kip1 stability and cellular localization*
**作者**：Slingerland J, Pagano M
**摘要**：文章探讨了重组CDKN1B蛋白在不同磷酸化状态下的稳定性及亚细胞定位变化，发现酪氨酸磷酸化通过促进泛素-蛋白酶体降解途径调控p27蛋白水平，从而影响细胞周期进程。
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3. **文献名称**：*Crystal structure of the p27Kip1 cyclin-dependent kinase inhibitor bound to the cyclin A-Cdk2 complex*
**作者**：Hengst L, et al.
**摘要**：该研究解析了重组p27蛋白与cyclin A-Cdk2复合物的晶体结构，阐明了其通过C端结构域与cyclin结合、N端与Cdk2相互作用的分子机制，为设计靶向细胞周期的药物提供了结构基础。
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CDKN1B, also known as p27 or KIP1. encodes a cyclin-dependent kinase (CDK) inhibitor critical for cell cycle regulation. As a member of the CIP/KIP protein family, p27 binds to and inhibits cyclin-CDK complexes, particularly cyclin E-CDK2 and cyclin D-CDK4/6. enforcing cell cycle arrest at the G1/S transition. This tumor suppressor protein integrates extracellular signals (e.g., growth factors, contact inhibition) with intracellular processes, balancing cell proliferation and quiescence. Its expression is tightly controlled through transcriptional regulation, protein stability (mediated by ubiquitin-proteasome degradation), and subcellular localization.
Recombinant CDKN1B protein is engineered using bacterial or mammalian expression systems to produce purified, functional p27 for experimental applications. Researchers utilize this recombinant protein to study cell cycle mechanisms, drug responses, and cancer biology. In vitro, it helps characterize interactions with CDKs, cyclins, and regulatory kinases like AKT. Its role in tumor suppression makes it valuable for investigating carcinogenesis, as CDKN1B mutations or reduced expression correlate with various cancers (e.g., breast, prostate, neuroendocrine tumors). Pharmaceutical studies employ recombinant p27 to screen compounds targeting cell cycle pathways or to optimize gene therapy approaches.
The recombinant form offers advantages over endogenous protein extraction, including batch consistency, scalability, and reduced contamination. Structural studies using recombinant CDKN1B have revealed phosphorylation-dependent conformational changes affecting its stability and activity. Emerging research explores its non-canonical roles in cytoskeletal regulation and apoptosis. However, challenges persist in maintaining proper post-translational modifications during recombinant production, which may influence functional studies. As a versatile tool, CDKN1B recombinant protein continues to advance our understanding of cell cycle control and therapeutic targeting in proliferative diseases.
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