Product Datasheet  
BCL10 Antibody  
Catalog Number: 32162  
Technical:tech@swbio.com  
Information:info@swbio.com  
Description  
  • host_species:  
  • Rabbit
  • Amount:  
  • 100μgμg
  • Swiss-Prot No.:  
  • Swiss-Prot:O95999
    NCBI Gene ID:8915
  • Form of Antibody:  
  • Supplied at 1.0mg/mL in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
  • Storage:  
  • Store at -20˚C
  • Immunogen:  
  • Recombinant protein of human BCL10.
  • reactivity:  
  • Human
  • appl_detail:  
  • WB 1:500 - 1:2000
  • other_names:  
  • BCL10; CARMEN; CIPER; CLAP; c-E10
  • Purification:  
  • Antibodies were purified by affinity purification using immunogen.
  • Specificity:  
  • The antibody detects endogenous level of total BCL10 protein.
  • Applications:  
  • WB
  • 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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