| 纯度 | > 90 % SDS-PAGE. |
| 种属 | Human |
| 靶点 | ADA1 |
| Uniprot No | P00813 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-363aa |
| 氨基酸序列 | MGSSHHHHHH SSGLVPRGSH MAQTPAFDKP KVELHVHLDG SIKPETILYY GRRRGIALPA NTAEGLLNVI GMDKPLTLPD FLAKFDYYMP AIAGCREAIK RIAYEFVEMK AKEGVVYVEV RYSPHLLANS KVEPIPWNQA EGDLTPDEVV ALVGQGLQEG ERDFGVKARS ILCCMRHQPN WSPKVVELCK KYQQQTVVAI DLAGDETIPG SSLLPGHVQA YQEAVKSGIH RTVHAGEVGS AEVVKEAVDI LKTERLGHGY HTLEDQALYN RLRQENMHFE ICPWSSYLTG AWKPDTEHAV IRLKNDQANY SLNTDDPLIF KSTLDTDYQM TKRDMGFTEE EFKRLNINAA KSSFLPEDEK RELLDLLYKA YGMPPSASAG QNL |
| 预测分子量 | 43 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ADA1重组蛋白的3篇示例参考文献(注：文献为模拟生成，实际引用请核实真实来源)：
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1. **文献名称**：*Recombinant ADA1 Enzyme Therapy for Severe Combined Immunodeficiency*
**作者**：Hershfield, M.S., et al.
**摘要**：研究利用重组ADA1蛋白治疗ADA缺乏型严重联合免疫缺陷症(SCID)，通过酶替代疗法改善患者免疫功能，并评估了长期治疗效果及安全性。
2. **文献名称**：*Expression and Purification of Human ADA1 in E. coli for Therapeutic Applications*
**作者**：Zhang, Y., et al.
**摘要**：报道了一种高效的大肠杆菌表达系统生产重组ADA1蛋白的方法，优化了纯化工艺，证实其酶活性和稳定性符合临床使用标准。
3. **文献名称**：*Structural Analysis of Recombinant ADA1 Using X-ray Crystallography*
**作者**：Johnson, R.L., et al.
**摘要**：通过X射线晶体学解析了重组ADA1的三维结构，揭示了其催化机制和底物结合位点，为开发新型ADA1突变体提供结构基础。
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如需真实文献，建议在PubMed或Google Scholar检索关键词：**"recombinant ADA1"**, **"adenosine deaminase therapy"**, **"ADA deficiency"**。
ADA1 recombinant protein is derived from adenosine deaminase 1 (ADA1), a critical enzyme in purine metabolism that catalyzes the irreversible deamination of adenosine and deoxyadenosine to inosine and deoxyinosine, respectively. ADA1 deficiency, an autosomal recessive disorder, causes severe combined immunodeficiency (SCID) due to the toxic accumulation of metabolites that impair lymphocyte development and function. Historically, SCID linked to ADA1 mutations was fatal in early childhood without intervention, driving research into therapeutic approaches like enzyme replacement therapy (ERT) and gene therapy.
Recombinant ADA1 is produced using biotechnological platforms, such as E. coli or mammalian expression systems, to ensure proper folding, post-translational modifications, and enzymatic activity. PEGylation—a process of attaching polyethylene glycol (PEG) chains—is often employed to enhance the protein’s stability, reduce immunogenicity, and prolong its circulating half-life. The PEGylated form, known as pegademase bovine (Adagen®), became the first FDA-approved enzyme replacement therapy for ADA-SCID in 1990. It provides systemic detoxification, restoring immune function in patients lacking endogenous ADA1.
Beyond ERT, recombinant ADA1 serves as a research tool to study immune regulation, nucleotide metabolism, and adenosine signaling pathways. It also holds potential in cancer immunotherapy, as adenosine accumulation in tumor microenvironments suppresses anti-tumor immunity. Inhibiting adenosine or supplementing ADA1 activity may counteract this immunosuppression. Additionally, recombinant ADA1 is explored in gene therapy protocols, where temporary enzyme support bridges the gap until genetically modified hematopoietic stem cells engraft. Its applications extend to diagnostic assays for ADA1 activity screening in newborns, aiding early detection of ADA-SCID. Overall, recombinant ADA1 represents a cornerstone in both therapeutic innovation and biomedical research.
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