Cell Signaling Technology

Product Pathways - NF-kB Signaling

Bcl10 (C78F1) Rabbit mAb #4237

Applications Reactivity Sensitivity MW (kDa) Isotype
W IP H M R (Mk) Endogenous 28 Rabbit IgG

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.

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.

Western Blotting

Western Blotting

Western blot analysis of extracts from Raji (human), A20 (mouse), and KNRK (rat) cell lines using Bcl10 (C78F1) Rabbit mAb.

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).

  1. Willis, T. G. et al. (1999) Cell 96, 35-45.
  2. Koseki, T. et al. (1999) J. Biol. Chem. 274, 9955-9961.
  3. Srinivasula, S. M. et al. (1999) J. Biol. Chem. 274, 17946-17954.
  4. Yan, M. et al. (1999) J. Biol. Chem. 274, 10287-10292.
  5. Zhang, Q. et al. (1999) Nature Genetics 22, 63-68.
  6. Ruland, J. et al. (2001) Cell 104, 33-42.
  7. Scharschmidt, E. et al. (2004) Mol. Cell. Biol. 24, 3860-3873.

Application References

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Companion Products

For Research Use Only. Not For Use In Diagnostic Procedures.

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