**Background of ARL9 Recombinant Protein**
ARL9 (ADP-ribosylation factor-like protein 9) is a member of the ARF/ARL family of small GTP-binding proteins, which play critical roles in intracellular trafficking, membrane remodeling, and organelle dynamics. These proteins act as molecular switches, cycling between inactive GDP-bound and active GTP-bound states to regulate vesicle formation, cargo sorting, and cytoskeletal organization. ARL9. though less characterized compared to other ARF/ARL members, shares structural features typical of the family, including conserved GTPase domains and effector-binding regions.
The recombinant ARL9 protein is engineered through genetic cloning and expression in heterologous systems (e.g., *E. coli* or mammalian cells*), enabling large-scale production of purified, functional protein for research. Recombinant technology allows precise control over post-translational modifications and avoids contamination from native cellular proteins. This has facilitated studies on ARL9's biochemical properties, such as GTP hydrolysis kinetics, interaction partners, and subcellular localization.
Emerging evidence suggests ARL9 may influence cellular processes linked to lysosomal function, autophagy, or signaling pathways. Dysregulation of ARF/ARL proteins is often associated with diseases like cancer, neurodegeneration, or ciliopathies, positioning ARL9 as a potential therapeutic or diagnostic target. Recombinant ARL9 serves as a vital tool for structural studies (e.g., crystallography), functional assays, and antibody development, helping to unravel its physiological and pathological roles. Ongoing research aims to clarify its specific mechanisms and relevance in human health, leveraging recombinant protein tools to bridge gaps in understanding this enigmatic GTPase.
以下是关于ARMC10重组蛋白的3篇参考文献(基于现有研究领域推测，供参考)：
1. **文献名称**：*ARMC10 regulates mitochondrial dynamics and promotes colorectal cancer metastasis*
**作者**：Wang, Y., et al.
**摘要**：本研究利用重组ARMC10蛋白进行功能实验，发现其通过调控线粒体分裂/融合动态，激活MAPK信号通路，从而促进结直肠癌细胞迁移和侵袭，为癌症治疗提供潜在靶点。
2. **文献名称**：*Structural and functional characterization of recombinant human ARMC10 in apoptosis regulation*
**作者**：Zhang, L., et al.
**摘要**：作者通过大肠杆菌表达系统纯化重组ARMC10蛋白，结合结构分析发现其通过Armadillo结构域与Bcl-2家族蛋白互作，调控线粒体依赖性细胞凋亡，揭示了其在癌症中的双重作用机制。
3. **文献名称**：*ARMC10 interacts with PINK1 to mediate mitophagy in neuronal cells*
**作者**：Chen, H., et al.
**摘要**：该研究利用重组ARMC10蛋白及基因敲除模型，证明其与PINK1协同参与线粒体自噬过程，维持神经元线粒体稳态，为神经退行性疾病研究提供新方向。
**注意**：以上文献为模拟示例，实际文献需通过PubMed或Web of Science检索。建议使用关键词“ARMC10 recombinant protein”或“ARMC10 mitochondrial function”查询最新研究。
ARMC10 (Armadillo repeat-containing protein 10) is a member of the Armadillo (ARM) repeat protein family, characterized by tandem repeats of approximately 40 amino acids that form a conserved helical structure. These proteins typically mediate protein-protein interactions and participate in diverse cellular processes, including signal transduction, cytoskeletal organization, and intracellular trafficking. ARMC10 is evolutionarily conserved and widely expressed in human tissues, with notable presence in the brain, liver, and kidneys. It localizes to mitochondria, where it regulates mitochondrial dynamics and function by interacting with fusion/fission machinery components. Dysregulation of ARMC10 has been linked to mitochondrial fragmentation, metabolic stress, and apoptosis, implicating its role in neurodegenerative diseases, cancer, and metabolic disorders.
Recombinant ARMC10 protein is engineered for functional and structural studies. Produced via heterologous expression systems (e.g., E. coli, HEK293. or insect cells), it retains post-translational modifications when expressed in eukaryotic systems, enhancing biological relevance. Purification techniques like affinity chromatography ensure high purity for applications such as antibody production, protein interaction assays (e.g., pull-downs, co-IP), and mitochondrial function studies. Research using recombinant ARMC10 has revealed its involvement in cancer progression, particularly in glioblastoma and hepatocellular carcinoma, where it modulates cell proliferation, migration, and chemoresistance. In neurodegenerative contexts, ARMC10 deficiency exacerbates mitochondrial dysfunction, suggesting therapeutic potential. Current efforts focus on targeting ARMC10 pathways to restore mitochondrial homeostasis or disrupt cancer-specific signaling. However, its exact molecular mechanisms remain under investigation, necessitating further exploration of its interactome and disease-specific roles.
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