| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 1/20 | Human,Mouse,Rat |
| IHC | 咨询技术 | Human,Mouse,Rat |
| ICC | 1/50-1/200 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 咨询技术 | Human,Mouse,Rat |
| Aliases | CBL; CBL2; RNF55; E3 ubiquitin-protein ligase CBL; Casitas B-lineage lymphoma proto-oncogene; Proto-oncogene c-Cbl; RING finger protein 55; Signal transduction protein CBL |
| Entrez GeneID | 867 |
| WB Predicted band size | Calculated MW: 100 kDa; Observed MW: 120 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 |
| Immunogen | A synthetic peptide of human CBL |
| Formulation | Purified antibody in TBS with 0.05% sodium azide,0.05%BSA and 50% glycerol. |
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以下是3篇与CBL抗体相关的经典文献摘要概括：
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1. **文献名称**：*Cbl: Many adaptations to regulate protein tyrosine kinases*
**作者**：Thien, C.B., Langdon, W.Y. (2001)
**摘要**：该综述系统总结了CBL蛋白的结构域及其作为E3泛素连接酶在调控受体酪氨酸激酶(RTKs)信号通路中的作用，重点讨论了CBL通过泛素化标记靶蛋白(如EGFR)促进其降解的机制，并提及相关抗体的应用(如免疫沉淀和Western blot)。
2. **文献名称**：*Cbl-mediated ubiquitination regulates EGFR endocytosis and MAPK signaling*
**作者**：Swaminathan, G., Alexander, D.R. (2003)
**摘要**：研究通过CBL抗体和突变实验，证明CBL蛋白介导的EGFR泛素化是其内吞和溶酶体降解的关键步骤，并揭示CBL缺失会导致EGFR信号过度激活，促进细胞增殖和肿瘤发生。
3. **文献名称**：*CBL mutations in human cancer: Prognostic and therapeutic implications*
**作者**：Kales, S.C., et al. (2010)
**摘要**：分析了白血病和实体瘤中CBL基因突变(如RING结构域突变)的临床意义，研究利用特异性CBL抗体检测患者样本，发现突变型CBL失去泛素连接酶活性，导致JAK2等激酶持续激活，提示其作为治疗靶点的潜力。
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以上文献涵盖了CBL的分子机制、信号调控及疾病关联，涉及抗体在功能研究(如蛋白互作、表达检测)中的应用。如需具体实验方法或抗体品牌，可进一步查阅原文方法学部分。
The Casitas B-lineage lymphoma (CBL) family of proteins, including CBL, CBLB, and CBLC, are evolutionarily conserved E3 ubiquitin ligases that play critical roles in regulating intracellular signaling pathways. Initially identified as a proto-oncogene due to its homology with the v-Cbl oncogene in retroviruses, CBL proteins function as negative regulators of receptor tyrosine kinases (RTKs) and other signaling molecules. They mediate the ubiquitination of activated receptors, targeting them for lysosomal or proteasomal degradation, thereby modulating cellular processes like proliferation, differentiation, and apoptosis.
CBL mutations or dysregulation have been implicated in various cancers, including myeloid neoplasms and solid tumors. Gain-of-function mutations in CBL can lead to constitutive activation of signaling pathways (e.g., RAS/MAPK, PI3K/AKT), while loss-of-function mutations impair its tumor-suppressive role. Additionally, CBL proteins interact with adaptor molecules (e.g., GRB2) and influence immune cell signaling, linking them to autoimmune diseases and immune dysregulation.
Antibodies targeting CBL are essential tools for studying its expression, post-translational modifications (e.g., phosphorylation), and interactions in both physiological and pathological contexts. They enable researchers to investigate CBL's dual roles as a tumor suppressor or oncogene, depending on cellular context and mutation status. Such antibodies are widely used in techniques like Western blotting, immunoprecipitation, and immunohistochemistry, aiding in the development of therapeutic strategies targeting CBL-associated pathways.
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