Anti-Mouse Bcl-3 Purified

Description: The Ham150-3.5 antibody reacts with mouse and human Bcl-3. Bcl-3 is a member of the IκB multigene family, which modulates the activities of NF-κB/Rel transcription factors. Bcl-3 is reported to increase transcription from NF-κB responsible promoters and to dissociate p50-p52 homodimers from DNA. Bcl-3 is phosphorylated influencing its interaction with both p50 and p52. Bcl-3 was cloned from a chromosomal breakpoint in the t(14;19) translocation, which is found in some cases of chronic B-cell lymphocytic leukemias. Bcl-3 is required for T-cell-dependent immunity. Bcl-3-deficient mice are defective in antigen-specific antibody production and germinal-center formation and fail to resist infection. Bcl-3 may also contribute to B-cell survival, which may explain its oncogenic potential when expressed at high levels as result of chromosomal translocation. Bcl-3 is detected in different tissues, especially the spleen and other lymphoid organs. The gene was shown to be induced by mitogenic stimuli in B and T cells and by cytokines on human erythroid precursors. It is shown that Bcl-3 expression is able to block apoptosis in IL-4-deprived cells.

References:
Rebollo A, Dumoutier L, Renauld JC, Zaballos A, Ayllon V, Martinez-A C. 2000. Bcl-3 expression promotes cell survival following interleukin-4 deprivation and is controlled by AP1 and AP1-like transcription factors. Mol Cell Biol. 20(10):3407-16.
Mitchell TC, Teague TK, Hildeman DA, Bender J, Rees WA, Kedl RM, Swanson B, Kappler JW, Marrack P. 2002. Stronger correlation of bcl-3 than bcl-2, bcl-xL, costimulation, or antioxidants with adjuvant-induced T cell survival. Ann N Y Acad Sci. 975:114-31.
Mitchell TC, Hildeman D, Kedl RM, Teague TK, Schaefer BC, White J, Zhu Y, Kappler J, Marrack P. 2001. Immunological adjuvants promote activated T cell survival via induction of Bcl-3. Nat Immunol. 2(5):397-402.