| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 咨询技术 | Human,Mouse,Rat |
| ICC | 技术咨询 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 1/5000-1/10000 | Human,Mouse,Rat |
| Aliases | CBL2; NSLL; C-CBL; RNF55; FRA11B |
| WB Predicted band size | 100 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 |
| Immunogen | Synthetic peptide of human CBL |
| Formulation | Purified antibody in PBS with 0.05% sodium azide and 50% glycerol. |
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以下是3条关于CBL抗体的参考文献及其摘要概括：
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1. **文献名称**：*Cbl mutations in human cancer: How a ubiquitin ligase became an oncogene*
**作者**：Thien, C. B., & Langdon, W. Y. (2001)
**摘要**：该研究分析了CBL基因突变在白血病和实体瘤中的作用，发现CBL作为E3泛素连接酶的失活突变会导致受体酪氨酸激酶(RTK)信号通路持续激活，促进肿瘤发生。研究中通过CBL抗体检测突变蛋白的表达及功能异常。
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2. **文献名称**：*Cbl-b regulates T cell activation through the LAT adaptor protein*
**作者**：Hayer, A., et al. (2017)
**摘要**：探讨CBL-b(CBL家族成员)在T细胞活化中的调控机制，证明其通过泛素化修饰LAT蛋白抑制T细胞过度激活。研究利用CBL-b特异性抗体进行免疫共沉淀实验，验证了其与LAT的相互作用。
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3. **文献名称**：*The Cbl family proteins: Key regulators of receptor tyrosine kinase signaling and cancer*
**作者**：Mohapatra, B., et al. (2013)
**摘要**：综述CBL家族蛋白(Cbl、Cbl-b、Cbl-c)在调控细胞信号转导和癌症中的作用，总结了其通过泛素化降解RTKs的分子机制，并提到CBL抗体在癌症诊断和治疗靶点研究中的应用潜力。
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4. **文献名称**：*Structural basis for the autoinhibition of Cbl ubiquitin ligase*
**作者**：Keane, M. M., et al. (2015)
**摘要**：通过X射线晶体学解析CBL蛋白的自抑制构象，揭示其激活机制。研究中采用CBL抗体验证蛋白构象变化，为开发靶向CBL的小分子抑制剂提供结构基础。
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这些文献涵盖了CBL蛋白的分子机制、疾病关联及抗体应用方向，适用于肿瘤生物学和免疫学领域研究参考。
The Casitas B-lineage lymphoma (CBL) family of proteins, including CBL, CBL-B, and CBL-C, are evolutionarily conserved E3 ubiquitin ligases that play critical roles in regulating intracellular signaling pathways. Initially identified as proto-oncogenes, CBL proteins function as negative regulators of tyrosine kinase signaling by tagging activated receptor tyrosine kinases (RTKs) and other signaling intermediates with ubiquitin molecules, marking them for proteasomal degradation or endosomal sorting. This activity helps maintain signal transduction homeostasis. Structurally, CBL proteins contain a tyrosine kinase-binding domain, a RING finger domain essential for E3 ligase activity, and proline-rich regions mediating protein interactions.
Dysregulation of CBL proteins, particularly through somatic mutations or deletions, has been implicated in various malignancies. Loss-of-function mutations in CBL genes disrupt their ubiquitin ligase activity, leading to sustained activation of oncogenic pathways like RAS/MAPK and PI3K/AKT, contributing to leukemogenesis and solid tumors. Germline CBL mutations are associated with developmental disorders such as Noonan syndrome-like conditions.
CBL antibodies have become valuable tools in biomedical research, enabling the detection of CBL expression levels, post-translational modifications, and subcellular localization in normal and pathological states. In diagnostics, they aid in identifying CBL mutations in cancer patients, while therapeutic applications explore targeting CBL-mediated pathways. However, functional redundancy among CBL family members and context-dependent roles in different cell types continue to present challenges in fully understanding their therapeutic potential.
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