| 纯度 | >85%SDS-PAGE. |
| 种属 | Human |
| 靶点 | DOCK3 |
| Uniprot No | Q8IZD9 |
| 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DOCK3重组蛋白的模拟参考文献示例，基于该领域常见研究方向构建：
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1. **文献名称**：*DOCK3 Recombinant Protein Promotes Axonal Regeneration via Rac1 Activation in Neuronal Cells*
**作者**：Kulkarni, S. et al. (2019)
**摘要**：本研究通过表达并纯化DOCK3重组蛋白，发现其通过激活Rac1 GTP酶显著增强体外培养神经元的轴突生长能力，为神经损伤修复提供了潜在治疗策略。
2. **文献名称**：*Structural and Functional Analysis of DOCK3 Reveals Its Role in Cancer Cell Migration*
**作者**：Miyamoto, T. et al. (2015)
**摘要**：利用重组DOCK3蛋白进行功能实验，证明其通过调控细胞骨架重组促进癌细胞迁移，且其N端结构域对结合下游信号分子至关重要。
3. **文献名称**：*DOCK3 Recombinant Protein Rescues Synaptic Deficits in a Neurodegenerative Model*
**作者**：Chen, L. et al. (2021)
**摘要**：在阿尔茨海默病模型中，重组DOCK3蛋白恢复了突触功能并减少tau蛋白过度磷酸化，表明其在神经退行性疾病中的治疗潜力。
4. **文献名称**：*Biochemical Characterization of DOCK3-ELMO1 Complex Using Recombinant Proteins*
**作者**：Yamauchi, A. et al. (2020)
**摘要**：通过重组DOCK3和ELMO1蛋白的体外结合实验，揭示了二者复合物的形成机制及其对Rac1信号通路的协同调控作用。
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**注**：以上文献为模拟内容，实际研究中请通过学术数据库(如PubMed、Web of Science)检索具体文献。
DOCK3 (dedicator of cytokinesis 3), also known as modifier of cell adhesion (MOCA), is a member of the DOCK protein family, which functions as atypical guanine nucleotide exchange factors (GEFs) for Rho GTPases. Specifically, DOCK3 belongs to the DOCK-A subfamily and primarily activates Rac1. a key regulator of cytoskeletal dynamics, cell migration, and neuronal signaling. Unlike classical GEFs, DOCK3 lacks the canonical Dbl homology (DH) domain but contains conserved DOCK homology regions (DHR1 and DHR2) that mediate membrane association and Rac1 activation, respectively.
Originally identified for its role in neuronal development, DOCK3 is highly expressed in the central nervous system, where it regulates axon guidance, synaptic plasticity, and myelination. Studies have linked DOCK3 dysfunction to neurodegenerative disorders, including Alzheimer’s disease, and spinal cord injuries, highlighting its importance in neuronal repair and survival. Beyond the nervous system, DOCK3 also influences cancer cell invasiveness and metastasis by modulating Rac1-dependent cytoskeletal remodeling.
Recombinant DOCK3 protein, produced via heterologous expression systems (e.g., bacterial, insect, or mammalian cells), enables mechanistic studies of its GEF activity, interactions with signaling partners (e.g., ELMO1/2. CrkII), and downstream pathways. Structural analyses of recombinant DOCK3 have clarified its autoinhibitory conformation and activation mechanisms, providing insights into targeted therapeutic strategies. For instance, small molecules or peptides disrupting DOCK3-ELMO or DOCK3-Rac1 interactions are being explored for treating neurological conditions or metastatic cancers.
Despite progress, challenges remain in understanding tissue-specific regulation of DOCK3 and its crosstalk with other Rho GEFs. Recombinant protein tools continue to drive discoveries in DOCK3 biology, bridging gaps between structural insights and disease-related applications.
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