BCL10 Antibody

This antibody is also available with the following conjugates:
AF350, AF405L, AF405M, AF405S, AF488, AF514, AF532, AF546, AF555, AF568, AF594, AF610, AF635, AF647, AF680, AF700, AF750, AF790, APC, AP, Biotin, Cy3, Cy5.5, Cy5, Cy7, FITC, HRP, PE, Magnetic beads (1 um, 2.8 um, 3 um, 4.5 um, 5 um, 10 um, 15 um, 20 um, 30 um, or different size option)
Please contact sales@hoelzel.de for pricing and availability.

26kDa

Affinity purification

Bcl10/CIPER/CLAP/mE10 is a widely expressed CARD (caspase recruitment domain) containing protein shown to induce apoptosis and activate NF-kappaB (1-5). The CARD domain mediates self-oligomerization, interactions with other CARD proteins and is necessary for NF-kappaB 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-kappaB 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-kappaBactiviation. PKC or T-cell receptor signaling results in a downregulation of Bcl10 protein levels, attenuating both NF-kappaB activation and cellular proliferation and also provides a negative feedback regulation of the NF-kappaB signaling to T cell signaling (7).