|Application ||WB, IHC|
|Calculated MW||62134 Da|
|Other Names||Transcription factor RelB, I-Rel, RELB|
|Target/Specificity||A synthetic peptide corresponding to residues in near the N-term of human RelB was used as immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||RelB Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||NF-kappa-B is a pleiotropic transcription factor which is present in almost all cell types and is involved in many biological processed such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF- kappa-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. NF-kappa-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-kappa-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF- kappa-B inhibitor (I-kappa-B) family. In a conventional activation pathway, I-kappa-B is phosphorylated by I-kappa-B kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NF-kappa-B complex which translocates to the nucleus. NF-kappa-B heterodimeric RelB-p50 and RelB-p52 complexes are transcriptional activators. RELB neither associates with DNA nor with RELA/p65 or REL. Stimulates promoter activity in the presence of NFKB2/p49. As a member of the NUPR1/RELB/IER3 survival pathway, may provide pancreatic ductal adenocarcinoma with remarkable resistance to cell stress, such as starvation or gemcitabine treatment. Regulates the circadian clock by repressing the transcriptional activator activity of the CLOCK-ARNTL/BMAL1 heterodimer in a CRY1/CRY2 independent manner. Increased repression of the heterodimer is seen in the presence of NFKB2/p52. Is required for both T and B lymphocyte maturation and function (PubMed:26385063).|
|Cellular Location||Nucleus. Cytoplasm, cytoskeleton, microtubule organizing center, centrosome. Note=Colocalizes with NEK6 in the centrosome|
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Provided below are standard protocols that you may find useful for product applications.
RelB, also known as I-Rel, is a member of the Rel transcription factor family which also include; RelA-p65, c-Rel, NF-kB1 p100/52 and NF-kB2 p105/50 (1). Unlike other Rel-related protein, RelB does not bind to DNA or to inhibitor IkB, but is instead sequestered in the cytoplasm by precursor p100. Once p100 is processed, the p52/RelB complex translocates into the nucleus (2). RelB is also the transcription factor that has been associated most directly with dendritic cells (DCs) differentiation and function (3). It is upregulated and translocated into the nuclei of DC in response to various stimuli. RelB is also essential for generating a specific DC subset (CD11c +/CD11b +/CD8 -/Dec205 -) from hematopoietic stem cells (5).
1. Blank, V., P. Kourilsky, and A. Israel. 1992. Trends Biochem. Sci. 17:135-140.
2. Yilmaz ZB, Weih DS, Sivakumar V, Weih F. EMBO J. 2003;22: 121-130.
3. Clark, G. J., S. Gunningham, A. Troy, S. Vuckovic, and D. N. Hart. 1999. Immunology 98:189-196
4. Ammon C, Mondal K, Andreesen R, Krause SW. Biochem Biophys Res Commun. 2000;268: 99-105
5. Wu L, D'Amico A, Winkel KD, Suter M, Lo D, Shortman K. Immunity. 1998;9: 839-847.
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