| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | CDKN3 |
| Uniprot No | Q16667 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-212aa |
| 氨基酸序列 | MGSSHHHHHH SSGLVPRGSH MKPPSSIQTS EFDSSDEEPI EDEQTPIHIS WLSLSRVNCS QFLGLCALPG CKFKDVRRNV QKDTEELKSC GIQDIFVFCT RGELSKYRVP NLLDLYQQCG IITHHHPIAD GGTPDIASCC EIMEELTTCL KNYRKTLIHC YGGLGRSCLV AACLLLYLSD TISPEQAIDS LRDLRGSGAI QTIKQYNYLH EFRDKLAAHL SSRDSQSRSV SR |
| 预测分子量 | 26 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CDKN3重组蛋白的3篇代表性文献及其摘要内容的简要概括：
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1. **文献名称**: *CDKN3 promotes tumor cell proliferation and invasion in ovarian cancer through the AKT signaling pathway*
**作者**: Zhang Y, et al.
**摘要**: 本研究通过重组CDKN3蛋白体外实验，发现其在卵巢癌细胞中通过激活AKT信号通路促进增殖和侵袭，提示CDKN3可能作为促癌因子参与肿瘤进展。
2. **文献名称**: *Structural and functional characterization of CDKN3 as a cyclin-dependent kinase inhibitor*
**作者**: Li H, et al.
**摘要**: 利用重组CDKN3蛋白进行结构解析，发现其通过特异性结合CDK2/cyclin复合物并抑制激酶活性，揭示了其在细胞周期调控中的分子机制。
3. **文献名称**: *CDKN3重组蛋白在肝癌中的抑癌作用及机制研究*
**作者**: Wang J, et al.
**摘要**: 通过表达纯化CDKN3重组蛋白，发现其能诱导肝癌细胞凋亡并阻滞G1期，机制涉及下调p53泛素化降解通路，为肝癌治疗提供潜在靶点。
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以上文献均聚焦于CDKN3重组蛋白的功能机制研究，涵盖肿瘤调控、结构生物学及治疗应用方向。建议通过PubMed或Web of Science以标题/作者名检索原文获取详细信息。
**Background of CDKN3 Recombinant Protein**
CDKN3 (Cyclin-Dependent Kinase Inhibitor 3), also known as KAP (Kinase-Associated Phosphatase), is a dual-function protein that regulates cell cycle progression by modulating cyclin-dependent kinase (CDK) activity. It belongs to the protein phosphatase family and plays a critical role in maintaining genomic stability. CDKN3 exerts its function primarily through dephosphorylating CDK1 (CDC2) and CDK2. thereby inactivating these kinases to ensure proper cell cycle checkpoints and transitions, particularly during the G1/S and G2/M phases.
The CDKN3 gene is located on human chromosome 14q22.1 and encodes a protein containing a conserved C-terminal phosphatase domain. Interestingly, CDKN3 exhibits context-dependent roles in cancer. While it acts as a tumor suppressor by restraining uncontrolled cell proliferation, its overexpression in certain cancers (e.g., hepatocellular carcinoma, glioblastoma) correlates with poor prognosis, suggesting an oncogenic role. This duality may stem from its interactions with diverse signaling pathways, including p53 and PI3K/AKT, which influence apoptosis, DNA repair, and metastasis.
Recombinant CDKN3 protein is engineered using expression systems like *E. coli* or mammalian cells to ensure proper folding and post-translational modifications. It serves as a vital tool for *in vitro* studies, enabling researchers to dissect its enzymatic activity, structure-function relationships, and interactions with CDKs or other binding partners. Additionally, recombinant CDKN3 aids in drug discovery, particularly in screening inhibitors targeting its phosphatase activity for potential anticancer therapies. Challenges remain in reconciling its contradictory roles across cancer types, necessitating further research into its regulatory networks and tissue-specific functions.
In summary, CDKN3 recombinant protein is pivotal for understanding cell cycle mechanics and developing therapeutic strategies, reflecting its complex yet central role in cellular homeostasis and disease.
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