Bcl3 Antibody Summary
| Immunogen |
Synthetic peptide surrounding amino acid 424 of human Bcl-.
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| Clonality |
Polyclonal
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| Host |
Rabbit
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| Gene |
BCL3
|
| Purity |
Immunogen affinity purified
|
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Applications/Dilutions
| Dilutions |
|
| Application Notes |
Western blot analysis (2-4 ug/ml). Per researchers feedback, the antibody also works well in Immunoprecipation (10-20 ug/ml), and Immunohistochemistry (20-40 ug/ml). However, the optimal conditions should be determined individually. Detects 55-60 kDa Bcl-3 of human, mouse, and rat origins. Other species have not been tested.
|
Packaging, Storage & Formulations
| Storage |
Aliquot and store at -20C or -80C. Avoid freeze-thaw cycles.
|
| Buffer |
PBS (pH 7.2), 0.5% BSA and 30% Glycerol
|
| Preservative |
0.01% Thimerosal
|
| Concentration |
0.2 mg/ml
|
| Purity |
Immunogen affinity purified
|
Alternate Names for Bcl3 Antibody
- B-cell CLL/lymphoma 3
- B-cell leukemia/lymphoma 3
- B-cell lymphoma 3 protein
- B-cell lymphoma 3-encoded protein
- BCL-3
- BCL4
- chronic lymphatic leukemia protein
- D19S37
- Proto-oncogene BCL3
Background
The Ham150-3.5 antibody reacts with mouse and human Bcl-3. Bcl-3 is a member of the IkappaB multigene family, which modulates the activities of NF-kappaB/Rel transcription factors. Bcl-3 is reported to increase transcription from NF-kappaB 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.