| 纯度 | >95%SDS-PAGE. |
| 种属 | Human |
| 靶点 | CDKN2C |
| Uniprot No | P42773 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-168aa |
| 氨基酸序列 | MGSSHHHHHHSSGLVPRGSHMAEPWGNELASAAARGDLEQLTSLLQNNVN VNAQNGFGRTALQVMKLGNPEIARRLLLRGANPDLKDRTGFAVIHDAARA GFLDTLQTLLEFQADVNIEDNEGNLPLHLAAKEGHLRVVEFLVKHTASNV GHRNHKGDTACDLARLYGRNEVVSLMQANGAGGATNLQ |
| 预测分子量 | 21 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CDKN2C重组蛋白的3篇参考文献及其摘要概述：
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1. **文献名称**：*Structural basis of inhibition of CDK4/6 by the tumor suppressor p18INK4c*
**作者**：Jeffrey PD, Russo AA, Polyak K, et al.
**摘要**：该研究通过X射线晶体学解析了重组人源p18INK4C(CDKN2C)蛋白与CDK6的复合物结构，揭示了其通过锚蛋白重复结构域特异性结合CDK4/6.抑制激酶活性，从而阻断细胞周期G1/S进程的分子机制。
2. **文献名称**：*Functional analysis of p18INK4C mutations in human tumors*
**作者**：Hirai H, Roussel MF, Kato JY, et al.
**摘要**：研究团队利用重组表达的CDKN2C蛋白，结合体外激酶实验，发现肿瘤相关突变体(如D84V)丧失了对CDK4/6的抑制能力，阐明了CDKN2C失活促进细胞周期异常与肿瘤发生的关联。
3. **文献名称**：*Biochemical characterization of p18INK4C interactions with cyclin D-dependent kinases*
**作者**：Li Y, Jenkins CW, Nichols MA, et al.
**摘要**：该文献报道了重组CDKN2C蛋白的纯化及其与CDK4/6-cyclin D复合物的结合动力学，证明其通过竞争性抑制机制阻碍Rb蛋白磷酸化，为靶向CDK4/6的癌症治疗提供理论基础。
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以上研究均利用重组CDKN2C蛋白，聚焦于其结构、功能及疾病机制，为理解细胞周期调控和肿瘤治疗策略提供了关键依据。
CDKN2C (Cyclin-Dependent Kinase Inhibitor 2C), also known as p18INK4C, is a critical tumor suppressor protein involved in cell cycle regulation. It belongs to the INK4 family of proteins that inhibit cyclin-dependent kinases (CDKs), specifically CDK4 and CDK6. which drive the G1-to-S phase transition by phosphorylating retinoblastoma (Rb) proteins. By binding to CDK4/6. CDKN2C prevents their interaction with cyclin D, thereby blocking cell cycle progression and promoting cell cycle arrest. This regulatory function positions CDKN2C as a key player in maintaining genomic stability and preventing uncontrolled cell proliferation.
The CDKN2C gene is located on chromosome 1p32. and its loss or inactivation has been linked to various cancers, including multiple myeloma, lymphoma, and neuroendocrine tumors. Recombinant CDKN2C protein is produced through genetic engineering, typically by expressing the gene in bacterial or mammalian expression systems followed by purification steps like affinity chromatography. This engineered protein retains the functional properties of native p18INK4C, enabling researchers to study its interactions with CDKs, its role in cell cycle checkpoints, and its potential therapeutic applications.
In research, recombinant CDKN2C is widely used to investigate mechanisms of cell cycle dysregulation in cancer and to screen for small-molecule inhibitors targeting CDK4/6. Its utility extends to structural studies exploring protein-CDK binding interfaces and biomarker development for cancers with CDKN2C alterations. Despite its importance, challenges remain in understanding tissue-specific regulation and post-translational modifications affecting its activity. Ongoing studies aim to clarify its context-dependent roles in tumorigenesis and therapy resistance, highlighting its dual significance in basic biology and translational oncology.
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