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- 详细信息
- 技术资料
- 抗体英文名:
Bcl10 (C78F1) Rabbit mAb
- 抗原:
synthetic peptide corresponding to residues surrounding Ser60 of Bcl10
- 应用范围:
W, IP
- 级别:
详见MSDS文件
- 供应商:
CST
- 保质期:
详见说明书
- 库存:
大量
- 适应物种:
H,M,R,Mk
- 是否单克隆:
1
- 保存条件:
-20°c
- 规格:
100 ul (10 western blots)/carrier free & custom formulation / quantity
| 规格: | 产品价格: | ¥请询价 | |
|---|---|---|---|
| 规格: | 100 ul (10 western blots) | 产品价格: | ¥请询价 |
| 规格: | carrier free & custom formulation / quantity | 产品价格: | ¥请询价 |
pathway more info application references datasheet PDF MSDS PDF protocols
Applications Key: W=Western Blotting IP=Immunoprecipitation
Reactivity Key: H=Human M=Mouse R=Rat Mk=Monkey
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.
| Applications | Reactivity | Sensitivity | MW (kDa) | Isotype |
|---|---|---|---|---|
| W IP | H M R (Mk) | Endogenous | 28 | Rabbit IgG |
| Protocols |
|
|---|---|
| Specificity / Sensitivity | Bcl10 (C78F1) Rabbit mAb detects endogenous levels of total Bcl10 protein. |
| Source / Purification | Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Ser60 of Bcl10. |
| Background | Bcl10/CIPER/CLAP/mE10 is a widely expressed CARD (caspase recruitment domain) containing protein shown to induce apoptosis and activate NF-κB (1-5). The CARD domain mediates self-oligomerization, interactions with other CARD proteins and is necessary for NF-κB activation, although the precise mechanism which Bcl10 regulates these processes is not fully understood. The discovery of Bcl10 came from observations of the chromosomal translocation t(1;14)(p22;q32) from B cell lymphomas of the mucosa-associated lymphoid tissue (MALT) (1,5). This translocation results in deregulated expression of a truncated form of Bcl10 which lacks apoptotic activity and enhances transformation. Studies from Bcl10 deficient mice demonstrate that Bcl10 is essential for the activation of NF-κB by T- and B-cell receptors (6). One third of Bcl10 deficient mice developed lethal exencephaly. Surviving mice were unaffected by various apoptotic stimuli, but were severely immunodeficient and defective in antigen receptor-induced NF-κB activiation. PKC or T-cell receptor signaling results in a downregulation of Bcl10 protein levels, attenuating both NF-κB activation and cellular proliferation and also provides a negative feedback regulation of the NF-κB signaling to T cell signaling (7).
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| Application References | Have you published research involving the use of our products? If so we'd love to hear about it. Please let us know ! |
| Companion Products |
For Research Use Only. Not For Use In Diagnostic Procedures. |
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