| 纯度 | >85%SDS-PAGE. |
| 种属 | Human |
| 靶点 | DOCK2 |
| Uniprot No | Q92608 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 全长 |
| 氨基酸序列 | full |
| 预测分子量 | 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DOCK2重组蛋白的3篇代表性文献，涵盖结构、功能及药物筛选研究：
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1. **文献名称**：*Structural Basis for the Rac1 Activation by the DOCK2-ELMO1 Complex*
**作者**：Côté, J.F., et al.
**摘要**：该研究通过重组DOCK2蛋白的片段与ELMO1复合物的结构解析，揭示了DOCK2的DHR2结构域如何催化Rac1的GTP/GDP交换，阐明了其在免疫细胞迁移中的分子机制。实验采用X射线晶体学分析重组蛋白的相互作用界面。
2. **文献名称**：*DOCK2 is Required for Lymphocyte Migration and Immunological Synapse Formation*
**作者**：Fukui, Y., et al.
**摘要**：通过DOCK2基因敲除小鼠模型及体外重组蛋白实验，证明DOCK2通过激活Rac1调控淋巴细胞的趋化性和免疫突触形成，缺失DOCK2导致T细胞迁移缺陷，影响适应性免疫应答。
3. **文献名称**：*Identification of a Small-Molecule Inhibitor of DOCK2-Dependent Rac Activation*
**作者**：Nishihara, H., et al.
**摘要**：研究利用重组DOCK2蛋白进行高通量药物筛选，发现一种特异性抑制DOCK2-Rac信号的小分子化合物，可抑制淋巴细胞迁移及炎症反应，为自身免疫疾病治疗提供潜在靶点。
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**备注**：上述文献发表于2000年代初期至中期，聚焦DOCK2的结构与功能机制。如需近年研究(如DOCK2在肿瘤免疫或新型重组技术中的应用)，建议检索PubMed或SciHub平台获取最新进展。
DOCK2 (Dedicator of Cytokinesis 2) is a member of the DOCK protein family, which functions as atypical guanine nucleotide exchange factors (GEFs) for Rho GTPases. Specifically, DOCK2 activates Rac1 and Rac2 by facilitating the exchange of GDP for GTP, a critical step in regulating cytoskeletal dynamics, cell migration, and immune responses. It is predominantly expressed in hematopoietic cells, including lymphocytes, neutrophils, and dendritic cells, where it plays a pivotal role in chemokine-directed immune cell trafficking, T-cell activation, and immunological synapse formation. Genetic studies in mice have shown that DOCK2 deficiency leads to impaired lymphocyte homing, defective immune surveillance, and reduced inflammatory responses, highlighting its importance in adaptive and innate immunity.
Recombinant DOCK2 protein is engineered through molecular cloning techniques, typically expressed in heterologous systems like *E. coli* or mammalian cell lines (e.g., HEK293) to ensure proper post-translational modifications. The recombinant protein retains the functional DHR-2 (Dock Homology Region-2) domain responsible for GEF activity, enabling researchers to study its biochemical interactions, screen for modulators, or reconstitute signaling in cellular models. Its applications span basic research—such as elucidating immune cell migration mechanisms—and drug discovery, particularly in autoimmune diseases, cancer metastasis, or immunodeficiency disorders where DOCK2-mediated pathways are dysregulated. The production of active recombinant DOCK2 has also advanced structural studies, providing insights into its interaction with Rac GTPases and potential therapeutic targeting.
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