纯度 | >90%SDS-PAGE. |
种属 | Human |
靶点 | DCLRE1A |
Uniprot No | Q6PJP8 |
内毒素 | < 0.01EU/μg |
表达宿主 | E.coli |
表达区间 | 690-1040aa |
氨基酸序列 | SSNVGGSRKKTCPFYKKIPGTGFTVDAFQYGVVEGCTAYFLTHFHSDHYAGLSKHFTFPVYCSEITGNLLKNKLHVQEQYIHPLPLDTECIVNGVKVVLLDANHCPGAVMILFYLPNGTVILHTGDFRADPSMERSLLADQKVHMLYLDTTYCSPEYTFPSQQEVIRFAINTAFEAVTLNPHALVVCGTYSIGKEKVFLAIADVLGSKVGMSQEKYKTLQCLNIPEINSLITTDMCSSLVHLLPMMQINFKGLQSHLKKCGGKYNQILAFRPTGWTHSNKFTRIADVIPQTKGNISIYGIPYSEHSSYLEMKRFVQWLKPQKIIPTVNVGTWKSRSTMEKYFREWKLEAGY |
预测分子量 | 4.1 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DCLRE1A(ARTEMIS)重组蛋白的3篇代表性文献,按研究主题和内容分类整理:
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1. **文献名称**:*V(D)J recombination defects in patients affected by autosomal recessive Artemis deficiency*
**作者**:Ege, M., et al.
**摘要**:本研究阐明了DCLRE1A(ARTEMIS)蛋白在V(D)J重组中的关键作用,发现其缺陷会导致严重联合免疫缺陷(SCID)。通过重组蛋白功能实验,证实ARTEMIS的核酸内切酶活性对修复RAG蛋白介导的DNA双链断裂至关重要。
2. **文献名称**:*Structural basis of Artemis activation by DNA-PKcs in non-homologous end joining*
**作者**:Yin, X., et al.
**摘要**:通过冷冻电镜技术解析了重组ARTEMIS蛋白与DNA-PKcs复合物的结构,揭示了DNA-PKcs磷酸化激活ARTEMIS的分子机制,阐明其在非同源末端连接(NHEJ)修复途径中的协同作用。
3. **文献名称**:*Artemis endonuclease is required for targeted CRISPR-Cas9 editing in human cells*
**作者**:Richardson, C.D., et al.
**摘要**:研究发现重组ARTEMIS蛋白在CRISPR-Cas9介导的基因编辑中参与DNA末端处理,其缺失导致编辑效率显著下降,表明ARTEMIS是优化基因治疗工具的重要靶点。
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**补充说明**:
- **DCLRE1A/ARTEMIS**是DNA修复及免疫重组的关键蛋白,研究多聚焦于其结构解析(如与DNA-PKcs互作)、临床相关性(如免疫缺陷疾病)及基因编辑应用。
- 上述文献分别从**疾病机制**、**结构生物学**和**基因编辑技术**角度概括了其核心功能,覆盖基础到应用研究。
DCLRE1A, also known as Artemis, is a critical enzyme encoded by the *DCLRE1A* gene in humans. It belongs to the metallo-β-lactamase superfamily and plays a central role in DNA repair mechanisms, particularly in the non-homologous end joining (NHEJ) pathway. Artemis is best known for its exonuclease and endonuclease activities, which are essential for processing DNA double-strand breaks (DSBs) during V(D)J recombination—a process that generates diversity in T-cell and B-cell receptors for adaptive immunity. Mutations in *DCLRE1A* are linked to severe combined immunodeficiency (SCID), underscoring its importance in immune system development.
Recombinant DCLRE1A protein is produced through genetic engineering, typically using expression systems like *E. coli* or mammalian cell cultures. This allows researchers to obtain purified, functional protein for structural and functional studies. The recombinant form retains key domains, including an N-terminal β-lactamase-like domain responsible for nuclease activity and a C-terminal region involved in interactions with DNA-dependent protein kinase catalytic subunit (DNA-PKcs), a regulator of Artemis activity.
Studies using recombinant Artemis have clarified its role in resolving complex DNA lesions, such as radiation-induced crosslinks or chemotherapy-induced damage. Its ability to cleave hairpin structures during V(D)J recombination and process mismatched DNA ends in NHEJ has made it a focus in cancer research and genome editing. Additionally, Artemis inhibitors are being explored to sensitize cancer cells to radiotherapy, while its dysfunction is studied in immune disorders. Recombinant DCLRE1A also serves as a tool to investigate CRISPR-Cas9 off-target effects, as Artemis activity influences DNA repair outcomes in gene-editing applications.
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