Recombinant Human Rel B protein
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Recombinant Human Rel B protein is a Human Full Length protein, expressed in Baculovirus infected Sf9 cells, with >85%, suitable for SDS-PAGE.
View Alternative Names
Transcription factor RelB, I-Rel, RELB
- SDS-PAGE
Unknown
SDS-PAGE - Recombinant Human Rel B protein (AB84654)
SDS-PAGE showing ab84654 at approximately 68kDa.
Reactivity data
Sequence info
Properties and storage information
Shipped at conditions
Appropriate short-term storage conditions
Appropriate long-term storage conditions
Aliquoting information
Storage information
Supplementary information
This supplementary information is collated from multiple sources and compiled automatically.
Biological function summary
Rel B serves as a critical component of the alternative NF-κB signaling pathway. It often forms a complex with another NF-κB family member called p52. This complex controls the transcription of genes involved in the immune response cell survival and differentiation. Additionally Rel B contributes to the development of secondary lymphoid organs and modulation of immune responses.
Pathways
Rel B integrates into the non-canonical NF-κB signaling pathway also influencing the canonical pathway to a lesser extent. In the non-canonical pathway Rel B interacts with NIK and p100 to influence immune cell function. This involvement makes Rel B essential in processes like adaptive immunity and inflammatory responses. The protein p52 closely associates with Rel B aiding its activity in these pathways.
Specifications
Form
Liquid
Additional notes
Affinity purified.
General info
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-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).
Post-translational modifications
Phosphorylation at 'Thr-103' and 'Ser-573' is followed by proteasomal degradation.
Subcellular localisation
Nucleus
Target data
Product promise
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