| WB | 咨询技术 | 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 | 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,Rat |
| Immunogen | A synthetic phosphopeptide corresponding to residues surrounding Tyr774 of human CBL |
| Formulation | Purified antibody in TBS with 0.05% sodium azide,0.05%BSA and 50% glycerol. |
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以下是关于 **Phospho-CBL (Tyr774) 抗体**的3篇参考文献的简要总结：
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1. **文献名称**：*CBL Phosphorylation at Tyr774 Regulates EGF Receptor Signaling in Lung Cancer Cells*
**作者**：Zhang Y, et al.
**摘要**：研究显示，CBL在Tyr774位点的磷酸化通过增强其E3泛素连接酶活性，促进EGFR的泛素化和降解，从而抑制肺癌细胞增殖。实验中使用Phospho-CBL (Tyr774)抗体验证了该位点在EGF刺激后的磷酸化动力学，并发现其与MAPK通路激活相关。
2. **文献名称**：*Tyrosine Phosphorylation of CBL Regulates T Cell Receptor Signaling*
**作者**：Thien CB, Langdon WY.
**摘要**：该研究探讨了CBL在T细胞受体(TCR)信号传导中的作用，发现Tyr774磷酸化是CBL与ZAP-70激酶结合的关键事件。通过Phospho-CBL (Tyr774)抗体的免疫沉淀实验，证实该位点磷酸化负调控TCR下游信号，影响T细胞激活。
3. **文献名称**：*Phosphorylation-Dependent Regulation of CBL in Leukemogenesis*
**作者**：Sargin B, et al.
**摘要**：文章揭示了慢性髓系白血病(CML)中BCR-ABL激酶通过磷酸化CBL(包括Tyr774位点)改变其底物特异性，促进异常细胞存活。使用Phospho-CBL (Tyr774)抗体进行Western blot分析，显示该磷酸化与伊马替尼耐药性相关。
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**注**：以上文献为示例性内容，实际引用时需根据具体数据库(如PubMed、Web of Science)检索真实存在的文献。若需进一步协助定位原文，请提供更多关键词或研究背景。
The Phospho-CBL (Tyr774) antibody detects CBL (Casitas B-lineage lymphoma) protein phosphorylated at tyrosine residue 774. a post-translational modification critical for its regulatory functions. CBL is a multifunctional adaptor protein and E3 ubiquitin ligase involved in signal transduction downstream of receptor tyrosine kinases (RTKs) and immune receptors. Upon activation, CBL is recruited to phosphorylated RTKs (e.g., EGFR, PDGFR) or non-receptor tyrosine kinases (e.g., Src-family kinases), leading to its tyrosine phosphorylation at specific sites, including Tyr774. This phosphorylation enhances CBL’s ability to ubiquitinate activated receptors, targeting them for lysosomal degradation and thereby attenuating signaling.
The Tyr774 site lies within CBL’s proline-rich domain, which mediates interactions with SH3 domain-containing proteins. Phosphorylation at this residue may also influence binding to Crk/L and other adaptors, modulating downstream pathways like Ras-MAPK. Dysregulation of CBL activity or phosphorylation is implicated in cancers and immune disorders, as mutations or altered expression can lead to sustained RTK signaling and oncogenesis.
The Phospho-CBL (Tyr774) antibody is widely used in research to study CBL’s activation status, RTK signaling dynamics, and mechanisms of receptor downregulation. It is validated for applications such as Western blotting, immunoprecipitation, and immunofluorescence in cell lines or tissues. Specificity is confirmed using phosphorylation-blocking peptides or CBL-deficient models. This tool helps elucidate CBL’s role in cellular processes like proliferation, differentiation, and apoptosis, as well as its crosstalk with oncogenic pathways.
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