Bcl10 (C78F1) Rabbit mAb #4237
- WB
- IP
Supporting Data
| REACTIVITY | H M R |
| SENSITIVITY | Endogenous |
| MW (kDa) | 28 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:50 |
Storage
Protocol
Specificity / Sensitivity
Bcl10 (C78F1) Rabbit mAb detects endogenous levels of total Bcl10 protein.
Species Reactivity:
Human, Mouse, Rat
The antigen sequence used to produce this antibody shares 100% sequence homology with the species listed here, but reactivity has not been tested or confirmed to work by CST. Use of this product with these species is not covered under our Product Performance Guarantee.
Species predicted to react based on 100% sequence homology:
Monkey
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).
- Willis, T.G. et al. (1999) Cell 96, 35-45.
- Koseki, T. et al. (1999) J Biol Chem 274, 9955-61.
- Srinivasula, S.M. et al. (1999) J Biol Chem 274, 17946-54.
- Yan, M. et al. (1999) J Biol Chem 274, 10287-92.
- Zhang, Q. et al. (1999) Nat Genet 22, 63-8.
- Ruland, J. et al. (2001) Cell 104, 33-42.
- Scharschmidt, E. et al. (2004) Mol Cell Biol 24, 3860-73.
Limited Uses
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