| WB | 1/500-1/1000 | Human,Mouse,Rat |
| IF | 1/20 | Human,Mouse,Rat |
| IHC | 咨询技术 | Human,Mouse,Rat |
| ICC | 技术咨询 | Human,Mouse,Rat |
| FCM | 1/50-1/100 | Human,Mouse,Rat |
| Elisa | 咨询技术 | Human,Mouse,Rat |
| Aliases | CUL3; KIAA0617; Cullin-3; CUL-3 |
| Entrez GeneID | 8452 |
| WB Predicted band size | Calculated MW: 89 kDa; Observed MW: 89 kDa |
| Host/Isotype | Rabbit IgG |
| Antibody Type | Primary antibody |
| Storage | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
| Species Reactivity | Human,Mouse,Rat |
| Immunogen | A synthesized peptide derived from human Cullin 3 |
| Formulation | Purified antibody in PBS with 0.05% sodium azide. |
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以下是关于Cullin 3抗体的模拟参考文献示例(仅供参考，实际文献需通过数据库验证)：
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1. **文献名称**：*CUL3-KLHL20 ubiquitin ligase complex regulates autophagy via degradation of ULK1*
**作者**：Huang, X., et al.
**摘要**：本研究利用Cullin 3抗体通过免疫共沉淀(Co-IP)和蛋白质印迹(WB)证实了CUL3与KLHL20形成的E3泛素连接酶复合体通过泛素化降解ULK1蛋白，负调控细胞自噬过程，揭示了其在癌症中的潜在作用。
2. **文献名称**：*Cullin 3 modulates blood pressure by ubiquitinating and degrading WNK kinases in renal cells*
**作者**：Ahn, J., et al.
**摘要**：通过Cullin 3抗体的免疫荧光染色和功能实验，研究发现Cullin 3通过泛素化降解WNK激酶调控肾脏离子通道活性，其突变可导致遗传性高血压，为相关疾病提供了分子机制解释。
3. **文献名称**：*Cullin 3 mutations impair RhoA degradation and promote cytoskeletal dysregulation in neurodevelopmental disorders*
**作者**：Chen, L., et al.
**摘要**：文章利用Cullin 3抗体在神经元细胞中验证了其与RhoA的相互作用，发现Cullin 3缺失导致RhoA异常积累，引发细胞骨架紊乱，提示其在神经系统发育疾病中的关键作用。
4. **文献名称**：*Antibody-based profiling of Cullin 3 substrates in neurodegenerative tauopathies*
**作者**：Smith, R., et al.
**摘要**：通过Cullin 3抗体的免疫沉淀结合质谱分析，鉴定出tau蛋白为Cullin 3泛素化底物，其异常修饰与阿尔茨海默病中神经纤维缠结的形成密切相关。
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**注意**：以上为模拟生成的参考文献，实际文献需通过PubMed/Google Scholar等平台检索确认。建议使用关键词“Cullin 3 antibody”或“Cullin 3 ubiquitin”查找最新研究。
Cullin 3 (CUL3) is a core component of the Cullin-RING ubiquitin ligase 3 (CRL3) complex, a critical regulator of the ubiquitin-proteasome system responsible for targeted protein degradation. As a scaffolding protein, CUL3 binds to RING-box proteins and substrate-recognition adaptors (e.g., BTB-domain proteins like KLHLs), facilitating the polyubiquitination of specific substrates for proteasomal breakdown. This process governs diverse cellular functions, including cell cycle progression, stress responses, and signal transduction. Dysregulation of CUL3 is linked to diseases such as hypertension (e.g., pseudohypoaldosteronism type II), cancer, and neurological disorders, underscoring its physiological importance.
CUL3 antibodies are essential tools for studying its expression, localization, and interactions in research. They enable techniques like Western blotting, immunohistochemistry, and co-immunoprecipitation to explore CRL3 complex dynamics or disease-associated CUL3 mutations. Specific antibodies may target distinct epitopes (e.g., N-terminal or C-terminal regions) to differentiate full-length CUL3 from truncated isoforms. Validation using knockout cells or tissues is critical to ensure specificity, as off-target binding can complicate interpretations. These antibodies have advanced understanding of CUL3’s roles in cellular homeostasis and pathology, supporting drug discovery efforts targeting ubiquitination pathways.
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