RELB
RELB (REL-B) is a Rel-like domain-containing subunit of the NF-kappa-B family of transcription factors. It forms heterodimers that regulate gene expression and is required for T and B lymphocyte maturation and function. Browse Assay Genie's current range of RELB research reagents below, or read on for the biology behind the target.
RELB is one of the Rel-like domain-containing proteins that assemble into NF-kappa-B, a pleiotropic transcription factor present in almost all cell types and involved in inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-kappa-B dimers bind kappa-B sites in the DNA of target genes, and individual dimers differ in their affinity and specificity for particular sites. Depending on the combination, dimers act as transcriptional activators or repressors. RELB-p50 and RELB-p52 heterodimers are transcriptional activators. RELB itself neither associates with DNA on its own nor pairs with RELA/p65 or REL, and it stimulates promoter activity in the presence of NFKB2/p49.
In the conventional activation pathway, NF-kappa-B complexes are held inactive in the cytoplasm by I-kappa-B inhibitors. I-kappa-B kinases phosphorylate I-kappa-B, which is then degraded, releasing NF-kappa-B to translocate to the nucleus. NF-kappa-B activity is also controlled by post-translational modification, subcellular compartmentalisation and interactions with cofactors or corepressors. UniProt places the RELB protein in the nucleus and at the centrosome, and NCBI Gene also reports it at chromatin and in the nucleoplasm. The RELB gene is a member of the HGNC groups for NF-kappa B complex subunits and IPT domain containing proteins; the mouse ortholog is Relb.
Beyond lymphocyte differentiation and negative regulation of interferon-beta production, RELB regulates the circadian clock by repressing CLOCK-BMAL1 heterodimer activity in a CRY1/CRY2-independent manner, an effect increased in the presence of NFKB2/p52. As part of the NUPR1/RELB/IER3 survival pathway, it may help pancreatic ductal adenocarcinoma resist cell stress such as starvation or gemcitabine. RELB is implicated in breast cancer and immunodeficiency 53, and is described as a biomarker of breast cancer and transitional cell carcinoma. Its earlier name was v-rel avian reticuloendotheliosis viral oncogene homolog B.
RELB is required for both T and B lymphocyte maturation and function, making it a focus in studies of immune cell differentiation.
RELB-p50 and RELB-p52 heterodimers act as transcriptional activators, so RELB is studied to dissect dimer-specific gene regulation within NF-κB pathways.
RELB is implicated in breast cancer, is a biomarker in breast cancer and transitional cell carcinoma, and sits in a pancreatic cancer survival pathway.
RELB represses CLOCK-BMAL1 transcriptional activity independently of CRY1/CRY2, linking NF-κB family signalling to circadian control.
RELB is an NF-kappa-B subunit that forms RelB-p50 and RelB-p52 heterodimers, which are transcriptional activators. It is required for T and B lymphocyte maturation and function, and it also represses CLOCK-BMAL1 activity to regulate the circadian clock.
The official HGNC name is RELB proto-oncogene, NF-kB subunit, and UniProt calls the protein transcription factor RelB. Aliases include REL-B. An earlier name was v-rel avian reticuloendotheliosis viral oncogene homolog B (nuclear factor of kappa light polypeptide gene enhancer in B-cells 3).
RELB is implicated in breast cancer and immunodeficiency 53, and is a biomarker of breast cancer and transitional cell carcinoma. The mouse ortholog is Relb. Check the datasheet of any product for its validated reactivity.
Other NF-κB family subunits, survival-pathway partners and circadian clock regulators that interact with RELB.
Gene and protein annotations from HGNC, NCBI Gene and UniProt Q01201; product specifications from Assay Genie datasheets.