| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | PRKN |
| Uniprot No | O60260 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-465aa |
| 氨基酸序列 | MIVFVRFNSSHGFPVEVDSDTSIFQLKEVVAKRQGVPADQLRVIFAGKELRNDWTVQNCDLDQQSIVHIVQRPWRKGQEMNATGGDDPRNAAGGCEREPQSLTRVDLSSSVLPGDSVGLAVILHTDSRKDSPPAGSPAGRSIYNSFYVYCKGPCQRVQPGKLRVQCSTCRQATLTLTQGPSCWDDVLIPNRMSGECQSPHCPGTSAEFFFKCGAHPTSDKETSVALHLIATNSRNITCITCTDVRSPVLVFQCNSRHVICLDCFHLYCVTRLNDRQFVHDPQLGYSLPCVAGCPNSLIKELHHFRILGEEQYNRYQQYGAEECVLQMGGVLCPRPGCGAGLLPEPDQRKVTCEGGNGLGCGFAFCRECKEAYHEGECSAVFEASGTTTQAYRVDERAAEQARWEAASKETIKKTTKPCPRCHVPVEKNGGCMHMKCPQPQCRLEWCWNCGCEWNRVCMGDHWFDV |
| 预测分子量 | 55.6 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PRKN(Parkin)重组蛋白的3篇代表性文献，涵盖结构、功能机制及应用研究：
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1. **文献名称**：*Structure of parkin reveals mechanisms for ubiquitin ligase activation*
**作者**：Trempe, J.-F., et al.
**摘要**：该研究通过X射线晶体学解析了重组Parkin蛋白的三维结构，揭示了其自抑制状态的构象及激活机制。研究发现，磷酸化修饰及与泛素结合可解除Parkin的自抑制，为帕金森病相关突变导致的酶活性丧失提供了分子解释。
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2. **文献名称**：*Phosphorylation of mitochondrial polyubiquitin by PINK1 activates Parkin*
**作者**：Kane, L.A., et al.
**摘要**：本文阐明了PINK1激酶通过磷酸化线粒体上的泛素链，触发重组Parkin的招募与激活，从而启动受损线粒体的自噬清除。研究证实了PINK1-Parkin信号轴在维持线粒体质量调控中的核心作用。
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3. **文献名称**：*Recombinant Parkin ameliorates α-synuclein toxicity in a rat model of Parkinson’s disease*
**作者**：Yasuda, T., et al.
**摘要**：通过腺相关病毒(AAV)递送重组Parkin蛋白至帕金森病大鼠模型，研究发现其可减少α-突触核蛋白的异常聚集，缓解神经元退行性病变及运动功能障碍，为Parkin的基因治疗潜力提供了实验依据。
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这些文献分别从结构生物学、分子机制及治疗应用的角度，解析了Parkin重组蛋白的功能与作用。如需更多近期研究，可进一步检索近年发表的Parkin相关蛋白工程或疾病模型论文。
Parkin (encoded by the PRKN gene) is an E3 ubiquitin ligase central to mitochondrial quality control and cellular homeostasis. Discovered in 1998 as a causative gene in autosomal recessive Parkinson’s disease (PD), Parkin plays a critical role in the PINK1/Parkin-mediated mitophagy pathway. Under stress, PINK1 accumulates on depolarized mitochondria, recruiting and activating Parkin to ubiquitinate outer membrane proteins, tagging damaged mitochondria for autophagic degradation. Dysfunctional Parkin due to PRKN mutations disrupts this process, leading to mitochondrial accumulation and neuronal degeneration, a hallmark of PD.
Recombinant Parkin proteins are engineered to study its structure-function relationships, mechanisms in mitophagy, and disease-related mutations. Produced via bacterial (e.g., E. coli) or eukaryotic systems (insect/mammalian cells), recombinant Parkin retains ubiquitin ligase activity when properly folded, though solubility and stability challenges often necessitate fusion tags (e.g., GST, His-tag) or co-expression with chaperones.
Research applications include in vitro assays to map substrate interactions, screen small molecules for PD therapy, and model pathogenic mutations. Structural studies using recombinant Parkin have revealed auto-inhibited conformations and activation steps triggered by phosphorylation. Despite progress, challenges persist in mimicking physiological conditions, such as post-translational modifications (e.g., phosphorylation by PINK1) critical for Parkin’s function.
Overall, recombinant Parkin remains a vital tool for deciphering PD pathogenesis and developing targeted therapies, bridging molecular insights to translational research.
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