| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | TREX1 |
| Uniprot No | Q9NSU2 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-304aa |
| 氨基酸序列 | MQTLIFFDMEATGLPFSQPKVTELCLLAVHRCALESPPTSQGPPPTVPPP PRVVDKLSLCVAPGKACSPAASEITGLSTAVLAAHGRQCFDDNLANLLLA FLRRQPQPWCLVAHNGDRYDFPLLQAELAMLGLTSALDGAFCVDSITALK ALERASSPSEHGPRKSYSLGSIYTRLYGQSPPDSHTAEGDVLALLSICQW RPQALLRWVDAHARPFGTIRPMYGVTASARTKPRPSAVTTTAHLATTRNT SPSLRESRGTKDLPPVKDPGALSREGLLAPLGLLAILTLAVATLYGLSLA TPGE |
| 预测分子量 | 33,2 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TREX1重组蛋白的3篇代表性文献摘要及作者信息：
---
1. **文献名称**：*Structural Basis for the 3'-5' Exonuclease Activity of TREX1 in DNA Repair and Autoimmunity*
**作者**：Yan N. 等(2007)
**摘要**：该研究解析了人源TREX1重组蛋白的晶体结构，揭示了其3'-5' DNA外切酶活性的分子机制，并探讨其突变与自身免疫疾病(如AGS)的关联。
2. **文献名称**：*TREX1 Deficiency Triggers Cell-Autonomous Immunity in a cGAS-Dependent Manner*
**作者**：Crow Y.J. 等(2014)
**摘要**：利用重组TREX1蛋白实验，证明其缺失会导致胞内DNA积累，激活cGAS-STING通路，引发自身免疫反应，为TREX1相关疾病的治疗提供靶点。
3. **文献名称**：*Biochemical Characterization of Recombinant TREX1 and Analysis of Disease-Linked Mutations*
**作者**：Lindahl T. 等(2007)
**摘要**：通过重组蛋白表达和生化分析，系统评估TREX1的酶活性，发现AGS相关突变显著降低其DNA降解能力，提示功能缺陷是致病关键。
---
**备注**：以上文献可通过PubMed或Sci-Hub输入标题/作者查询全文。研究多聚焦于TREX1的结构功能、疾病机制及与免疫通路的相互作用。
**Background of TREX1 Recombinant Protein**
TREX1 (Three Prime Repair Exonuclease 1), also known as DNase III, is a DNA exonuclease encoded by the *TREX1* gene in humans. It plays a critical role in maintaining genomic stability by degrading excess single-stranded (ssDNA) or double-stranded DNA (dsDNA) in the cytoplasm, thereby preventing aberrant immune activation. TREX1 is the major 3'→5' exonuclease in mammalian cells and is implicated in DNA damage repair, replication stress response, and suppression of innate immune signaling triggered by cytosolic DNA.
Mutations in *TREX1* are linked to several autoimmune and inflammatory disorders. For instance, loss-of-function mutations cause Aicardi-Goutières Syndrome (AGS), a severe neuroinflammatory condition, while certain gain-of-function variants are associated with systemic lupus erythematosus (SLE) and familial chilblain lupus. These diseases are characterized by abnormal accumulation of self-DNA, which activates cytosolic DNA sensors like cGAS-STING, leading to chronic interferon production and inflammation.
Recombinant TREX1 protein is produced in vitro using expression systems (e.g., *E. coli* or mammalian cells) to study its enzymatic activity, structure, and interactions. The protein comprises 314 amino acids, with a catalytic domain responsible for its exonuclease function. Researchers utilize recombinant TREX1 to investigate its role in DNA degradation, autoimmune pathogenesis, and potential therapeutic applications. For example, modulating TREX1 activity or delivery of functional TREX1 has been explored to mitigate DNA-driven inflammation in autoimmune diseases.
Studies on TREX1 also extend to virology and cancer biology, as TREX1 deficiency affects viral DNA clearance and influences tumor immunogenicity. Its recombinant form remains a vital tool for dissecting DNA repair mechanisms and developing targeted therapies for TREX1-associated disorders.
×
