| 纯度 | > 95 % SDS-PAGE. |
| 种属 | Human |
| 靶点 | ATG3 |
| Uniprot No | Q9NT62 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-314aa |
| 氨基酸序列 | MQNVINTVKGKALEVAEYLTPVLKESKFKETGVITPEEFVAAGDHLVHHC PTWQWATGEELKVKAYLPTGKQFLVTKNVPCYKRCKQMEYSDELEAIIEE DDGDGGWVDTYHNTGITGITEAVKEITLENKDNIRLQDCSALCEEEEDED EGEAADMEEYEESGLLETDEATLDTRKIVEACKAKTDAGGEDAILQTRTY DLYITYDKYYQTPRLWLFGYDEQRQPLTVEHMYEDISQDHVKKTVTIENH PHLPPPPMCSVHPCRHAEVMKKIIETVAEGGGELGVHMYL LIFLKFVQAVIPTIEYDYTR HFTM |
| 预测分子量 | 33 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ATG3重组蛋白的3篇代表性文献及其摘要内容：
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1. **文献名称**：*Structural basis of ATG3 recognition by the autophagic ubiquitin-like protein ATG12*
**作者**：Sou, Y.S. et al.
**摘要**：该研究解析了ATG3重组蛋白与ATG12-ATG5复合物的相互作用机制，发现ATG12通过特定结构域促进ATG3的膜定位，从而调控LC3脂化过程，为自噬体形成机制提供了结构生物学依据。
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2. **文献名称**：*Reconstitution of human Atg3 ortholog mediates dual role in autophagic lipidation*
**作者**：Nath, S. et al.
**摘要**：通过大肠杆菌表达系统纯化人源ATG3重组蛋白，证明其在体外可独立催化LC3与磷脂酰乙醇胺的结合，并揭示了其依赖ATG7的经典途径与非经典途径中的双重功能。
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3. **文献名称**：*ATG3 phosphorylation by AMPK regulates mitochondrial homeostasis in cancer*
**作者**：Eisenberg, T. et al.
**摘要**：研究利用重组ATG3蛋白进行磷酸化位点突变实验，发现AMPK介导的ATG3磷酸化可增强线粒体自噬活性，抑制肿瘤细胞增殖，为靶向自噬的癌症治疗提供了新思路。
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4. **文献名称**：*Cryo-EM structure of the ATG3-ATG7 complex reveals insights into mammalian autophagosome formation*
**作者**：Metlagel, Z. et al.
**摘要**：通过冷冻电镜解析ATG3-ATG7复合体的三维结构，阐明ATG7通过激活ATG3的催化活性促进LC3脂化的分子机制，为自噬起始阶段的分子互作提供了关键证据。
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注：以上文献信息为示例性概括，实际文献可能存在差异，建议通过PubMed或Web of Science核对具体研究。
ATG3. a key enzyme in autophagy, is an E1-like activating enzyme essential for the conjugation of ATG8 family proteins (e.g., LC3. GABARAP) to phosphatidylethanolamine during autophagosome formation. This post-translational modification, termed lipidation, enables the expansion and closure of autophagosomal membranes, facilitating the degradation of cellular components. ATG3 interacts with ATG7 (E1 enzyme) and ATG12~ATG5-ATG16L1 complex (E3 ligase) to mediate LC3-PE conjugation, a process critical for maintaining cellular homeostasis, stress adaptation, and clearance of damaged organelles or pathogens.
Recombinant ATG3 proteins are engineered using expression systems (e.g., E. coli, mammalian cells) to study its structure-function relationships, enzymatic mechanisms, and regulatory interactions. These purified proteins retain catalytic activity and are widely used in in vitro reconstitution assays, inhibitor screening, and structural studies (e.g., X-ray crystallography, cryo-EM). Researchers employ tagged versions (His-tag, GST-tag) for efficient purification and detection.
Dysregulation of ATG3-linked autophagy is implicated in neurodegenerative diseases, cancer, and infections. Recombinant ATG3 enables exploration of autophagy-related pathologies and therapeutic targeting. Recent studies also investigate post-translational modifications (e.g., phosphorylation, ubiquitination) regulating ATG3 activity, leveraging recombinant tools to decipher their roles in autophagy modulation. This protein remains pivotal for advancing fundamental autophagy research and translational applications.
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