DATASHEET
Host:
Mouse
Target Protein:
RELB
Clonality:
Monoclonal
Isotype:
IgG1
Entrez Gene:
5971
Swiss Prot:
Q01201
Source:
This RELB antibody is generated from a mouse immunized with a recombinant protein human RELB.
Purification:
Purified by Protein G.
Storage Buffer:
0.01M TBS(pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.
Storage:
Store at -20°C for 12 months.
Background:
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.
VALIDATION IMAGES
Lane 1: Raji; Lane 2: Jurkat; Lane 3: NIH/3T3 cell lysate at 20 µg per lane, probed with bsm-51381M RELB (4C5) Monoclonal Antibody at 1:5000 dilution and 4℃ overnight incubation, followed by secondary antibody incubation for 60min at room temperature.
Lane 1: Daudi Cell lysates; probed with RELB (4C5) Monoclonal Antibody, unconjugated (bsm-51381M) at 1:5000 overnight at 4°C followed by a conjugated secondary antibody for 60 minutes at 37°C.