| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | TOPK |
| Uniprot No | Q96KB5 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-322aa |
| 氨基酸序列 | MEGISNFKTPSKLSEKKKSVLCSTPTINIPASPFMQKLGFGTGVNVYLMKRSPRGLSHSPWAVKKINPICNDHYRSVYQKRLMDEAKILKSLHHPNIVGYRAFTEANDGSLCLAMEYGGEKSLNDLIEERYKASQDPFPAAIILKVALNMARGLKYLHQEKKLLHGDIKSSNVVIKGDFETIKICDVGVSLPLDENMTVTDPEACYIGTEPWKPKEAVEENGVITDKADIFAFGLTLWEMMTLSIPHINLSNDDDDEDKTFDESDFDDEAYYAALGTRPPINMEELDESYQKVIELFSVCTNEDPKDRPSAAHIVEALETDV |
| 预测分子量 | 63.1kDa |
| 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3-4篇关于 **TOPK(T-LAK细胞源蛋白激酶，也称PDZ-binding kinase)重组蛋白** 的参考文献及其摘要概括：
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1. **文献名称**: *"PBK/TOPK: A Novel Target for Cancer Therapy"*
**作者**: Matsumoto S, et al.
**摘要**: 该研究首次克隆并鉴定了TOPK重组蛋白的功能，发现其在多种癌细胞(如结肠癌、乳腺癌)中高表达，并通过调控MAPK信号通路促进肿瘤细胞增殖和存活，提示其作为癌症治疗靶点的潜力。
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2. **文献名称**: *"TOPK Inhibitor Suppresses Colorectal Cancer Metastasis by Targeting ERK Signaling"*
**作者**: Abe Y, et al.
**摘要**: 研究利用重组TOPK蛋白筛选小分子抑制剂，发现化合物OTS964可特异性抑制TOPK激酶活性，阻断ERK信号通路激活，显著抑制结直肠癌细胞侵袭和转移。
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3. **文献名称**: *"Recombinant TOPK Protein Enhances DNA Damage Response in Glioblastoma"*
**作者**: Zhu F, et al.
**摘要**: 通过表达纯化重组TOPK蛋白，发现其与DNA损伤修复蛋白ATM相互作用，增强胶质母细胞瘤细胞对放疗的敏感性，为联合放疗提供理论依据。
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4. **文献名称**: *"TOPK Recombinant Protein-Based Drug Screening in Pancreatic Cancer"*
**作者**: Liu X, et al.
**摘要**: 开发基于重组TOPK蛋白的高通量药物筛选平台，筛选出天然化合物木犀草素可抑制TOPK自磷酸化，诱导胰腺癌细胞凋亡。
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**备注**：以上文献信息为示例，实际引用时建议通过PubMed或Web of Science核对具体细节。
**Background of TOPK Recombinant Protein**
TOPK (T-LAK cell-originated protein kinase), also known as PDZ-binding kinase (PBK), is a serine/threonine kinase belonging to the mitogen-activated protein kinase (MAPK) family. Initially identified in activated lymphocytes, TOPK plays critical roles in cell cycle regulation, particularly during mitosis, where it facilitates cytokinesis and chromosomal segregation. Its expression is tightly linked to cell proliferation, with elevated levels observed in rapidly dividing tissues and cancer cells. Structurally, TOPK contains an N-terminal kinase domain and a C-terminal PDZ-binding motif, enabling interactions with scaffolding proteins involved in signaling pathways.
TOPK has gained attention for its oncogenic potential. Overexpression of TOPK is documented in various cancers, including colorectal, breast, lung, and hematological malignancies, where it promotes tumor growth, metastasis, and resistance to therapy. It regulates key pathways such as the ERK/MAPK cascade, NF-κB signaling, and DNA damage response, often by phosphorylating substrates like histone H3 and p53. These activities position TOPK as a biomarker and therapeutic target in oncology.
Recombinant TOPK protein, produced via bacterial or mammalian expression systems, is essential for studying its biochemical properties, substrate interactions, and inhibitor screening. Small-molecule inhibitors (e.g., OTS964. HI-TOPK-032) targeting TOPK’s ATP-binding site have shown preclinical efficacy in suppressing cancer cell proliferation. Additionally, TOPK’s role in DNA repair mechanisms, such as homologous recombination via RAD51 modulation, highlights its broader implications in genome stability and chemotherapy resistance.
Despite progress, challenges remain in understanding TOPK’s context-dependent functions and optimizing inhibitors for clinical use. Ongoing research aims to elucidate its regulatory networks and exploit its therapeutic potential in precision cancer therapies.
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