|Tested species reactivity||Human|
|Published species reactivity||Not Applicable|
|Host / Isotype||Rabbit / IgG|
|Immunogen||Synthetic peptides corresponding to residues 2-13 and 107-120 of human Bcl-3.|
|Storage buffer||PBS with 0.05% BSA|
|Contains||0.05% sodium azide|
|Storage Conditions||Store at 4°C short term. For long term storage, store at -20°C, avoiding freeze/thaw cycles.|
|Tested Applications||Dilution *|
|Western Blot (WB)||0.5-1 µg/ml|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
|Western Blot (WB)||See 1 publications below|
Suggested positive control: Jurkat whole cell lysate.
NF-kB is silenced in the cytoplasm by an inhibitory protein, IkB (1). The proto-oncoprotein Bcl-3 is a member of the IkB family and is present predominantly in the nucleus. IkBa and Bcl-3 are similar in the central ankyrin repeat domains, where as they differ at the N- and –C terminus. These differences may explain the differential binding of IkBa and Bcl-3. Two molecules of Bcl-3 can associate with NF-kB, where as only one molecule of IkBa bind to NF-kB. BCL-3 mRNA and protein expression are induced by NF-kB-activating agents. Down-regulation of BCL-3 induction results in prolonged, enhanced NF-kB binding and increased NF-kB-dependent transcription. Several cytokines, such as, TNFa or IL-1b, and mitogens as phorbolester (PMA) trigger rapid formation of Bcl-3-p50 complexes with the same kinetics as activation of p50-p65 complexes.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
|Not Applicable||Not Cited||
Regulation of p53 and Rb links the alternative NF-¿B pathway to EZH2 expression and cell senescence.
PA1-41087 was used in western blot to report that NF-kappaB2 and RelB have multiple effects on the expression of key regulators of the cell cycle, reactive oxygen species generation, and protein stability
|Iannetti A,Ledoux AC,Tudhope SJ,Sellier H,Zhao B,Mowla S,Moore A,Hummerich H,Gewurz BE,Cockell SJ,Jat PS,Willmore E,Perkins ND||PLoS genetics (10:null)||2014|