| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | CDKN2A |
| Uniprot No | Q96HQ2 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-116aa |
| 氨基酸序列 | MVGGEAAAAVEELVSGVRQAADFAEQFRSYSESEKQWKARMEFILRHLPDYRDPPDGSGRLDQLLSLSMVWANHLFLGCSYNKDLLDKVMEMADGIEVEDLPQFTTRSELMKKHQS |
| 预测分子量 | 17.2kDa |
| 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CDKN2A重组蛋白的3篇参考文献示例(内容基于模拟生成，具体文献需自行核实)：
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1. **文献名称**：*Structural and Functional Analysis of Recombinant CDKN2A/p16INK4a Protein in Tumor Suppression*
**作者**：Smith J, et al.
**摘要**：研究通过大肠杆菌表达系统纯化重组CDKN2A/p16INK4a蛋白，解析其与CDK4/6结合的晶体结构，证实其通过抑制细胞周期蛋白依赖性激酶阻断细胞周期进程的能力。
2. **文献名称**：*Recombinant p14ARF Protein Induces Apoptosis via p53 Stabilization in Cancer Cells*
**作者**：Li X, et al.
**摘要**：利用杆状病毒系统表达重组p14ARF蛋白，证明其通过结合MDM2稳定p53.触发癌细胞凋亡，为靶向治疗提供实验依据。
3. **文献名称**：*High-Yield Production of CDKN2A Isoforms for Drug Screening Platforms*
**作者**：Garcia R, et al.
**摘要**：优化哺乳动物细胞表达体系，实现p16INK4a和p14ARF的高效分泌表达，并应用于高通量筛选靶向CDKN2A通路的抗癌化合物。
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建议通过PubMed或Google Scholar检索关键词“CDKN2A recombinant protein”、“p16/p14ARF expression”获取最新文献。
CDKN2A (Cyclin-Dependent Kinase Inhibitor 2A) is a tumor suppressor gene located on chromosome 9p21.3. encoding two distinct proteins through alternative reading frames: p16INK4a and p14ARF (p19Arf in mice). These proteins regulate cell cycle progression and apoptosis, playing critical roles in preventing uncontrolled proliferation. p16INK4a inhibits cyclin-dependent kinases CDK4 and CDK6. blocking phosphorylation of retinoblastoma (Rb) protein and arresting the cell cycle at G1 phase. p14ARF stabilizes p53 by binding to MDM2. thereby promoting cell cycle arrest or apoptosis in response to oncogenic stress. Dysregulation of CDKN2A through mutations, deletions, or epigenetic silencing is implicated in various cancers, including melanoma, pancreatic cancer, and glioblastoma.
Recombinant CDKN2A proteins are engineered in vitro to study their functional mechanisms or potential therapeutic applications. These proteins are typically produced using expression systems (e.g., E. coli, mammalian cells) with affinity tags for purification. Recombinant p16INK4a and p14ARF serve as tools to investigate tumor suppression pathways, screen anticancer drugs, or analyze structural interactions with CDKs/MDM2. Their use in preclinical models has provided insights into restoring cell cycle control in CDKN2A-deficient cancers. However, challenges remain in delivery efficiency and stability for therapeutic use. Research continues to explore recombinant CDKN2A proteins as part of gene therapy or combination treatments targeting cell cycle dysregulation in oncology.
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