| 纯度 | > 90 % SDS-PAGE |
| 种属 | Human |
| 靶点 | ATG4B |
| Uniprot No | Q9Y4P1 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-393aa |
| 氨基酸序列 | MDAATLTYDT LRFAEFEDFP ETSEPVWILG RKYSIFTEKD EILSDVASRL WFTYRKNFPA IGGTGPTSDT GWGCMLRCGQ MIFAQALVCR HLGRDWRWTQ RKRQPDSYFS VLNAFIDRKD SYYSIHQIAQ MGVGEGKSIG QWYGPNTVAQ VLKKLAVFDT WSSLAVHIAM DNTVVMEEIR RLCRTSVPCA GATAFPADSD RHCNGFPAGA EVTNRPSPWR PLVLLIPLRL GLTDINEAYV ETLKHCFMMP QSLGVIGGKP NSAHYFIGYV GEELIYLDPH TTQPAVEPTD GCFIPDESFH CQHPPCRMSI AELDPSIAVG FFCKTEDDFN DWCQQVKKLS LLGGALPMFE LVEQQPSHLA CPDVLNLSLD SSDVERLERF FDSEDEDFEI LSLLEHHHHH H |
| 预测分子量 | 45 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ATG4B重组蛋白的3篇文献概览(内容基于领域内典型研究，部分信息为示例整合)：
1. **标题**：*Crystal structure of human ATG4B reveals a critical role of the N-terminal domain for its proteolytic activity*
**作者**：Maruyama T, Yoshimori T 等
**摘要**：该研究解析了人源ATG4B重组蛋白的晶体结构，发现其N端结构域对底物LC3的识别和切割至关重要，为理解自噬相关酶活调控机制提供了结构基础。
2. **标题**：*Characterization of recombinant ATG4B enzyme activity and its regulation by oxidative stress*
**作者**：Li M, et al.
**摘要**：通过体外表达纯化ATG4B重组蛋白，揭示了其切割LC3的动力学参数，并证明氧化应激通过修饰ATG4B的活性位点半胱氨酸抑制其功能。
3. **标题**：*Development of ATG4B inhibitors using high-throughput screening with recombinant protein*
**作者**：Satoo K, Noda NN 等
**摘要**：利用重组ATG4B蛋白建立高通量筛选平台，发现小分子抑制剂可阻断其蛋白酶活性，为抗肿瘤药物研发提供了新策略。
4. **标题**：*Phosphorylation of ATG4B modulates its subcellular localization and function in autophagy*
**作者**：Ronan B, et al.
**摘要**：研究通过重组蛋白突变实验，证明特定位点的磷酸化调控ATG4B的细胞定位及其在自噬体形成中的作用，关联了信号通路与自噬激活机制。
(注：以上文献标题及作者为领域相关研究方向示例，实际引用需以具体论文为准。)
ATG4B, also known as Autophagin-1 or cysteine protease ATG4B, is a key enzyme in the autophagy pathway, a conserved cellular process responsible for degrading and recycling damaged organelles, misfolded proteins, and pathogens. As a member of the ATG4 cysteine protease family, it plays a critical role in processing microtubule-associated protein 1A/1B-light chain 3 (LC3), a central component of autophagosome formation. Specifically, ATG4B cleaves the C-terminal region of pro-LC3 to generate LC3-I, which is subsequently conjugated to phosphatidylethanolamine (PE) on autophagosomal membranes (forming LC3-II). This lipidated form of LC3 enables autophagosome expansion and cargo recruitment. Additionally, ATG4B mediates the delipidation of LC3-II during late-stage autophagy, recycling LC3 for subsequent rounds of autophagosome formation.
Recombinant ATG4B protein is produced using expression systems like *E. coli* or mammalian cell lines, followed by purification to ensure high activity and specificity. Its structural features include a catalytic domain with conserved cysteine and histidine residues essential for protease activity, as well as regulatory regions influencing substrate recognition. Studies using recombinant ATG4B have advanced the understanding of autophagy dynamics, substrate specificity, and regulatory mechanisms. Dysregulation of ATG4B has been linked to diseases such as cancer, neurodegenerative disorders (e.g., Parkinson’s and Alzheimer’s), and metabolic syndromes, making it a potential therapeutic target. Inhibitors or activators of ATG4B are being explored to modulate autophagy in disease contexts. Furthermore, recombinant ATG4B serves as a vital tool for *in vitro* assays, drug screening, and structural studies to elucidate its interaction with LC3 homologs and other autophagy-related proteins. Its biochemical characterization continues to uncover novel roles in cellular stress responses and homeostasis.
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