RELB — RELB proto-oncogene, NF-kB subunit

RELB belongs to a gene co-expression module in 10 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.

RELB's module in each cell type

Cell type	Module	Shares the module with
CD4⁺ T cells	NF-kB activation TCR/AP1/NFKb pathway	ABCF1, BCL2A1, BUD23, BZW2, CALR, CEBPZ, DDX21, DENND4A +21 more	View in SCUBA
Endothelial	NF-κB Endothelial Activation Inflammation	LITAF, NAMPT, NFKB2, NUAK2, SBNO2, SELE, SLC35F2, SRGAP1 +5 more	View in SCUBA
Fibroblasts	ER Stress UPR Stress	ARF4, B4GALT1, BTG3, BZW1, CYCS, EFHD2, ELOC, LDHA +6 more	View in SCUBA
Gamma-delta T cells	NF-κB Activation Inflammation	DUSP5, GADD45A, HERPUD1, IL21R, KDM6B, MAFF, NAMPT, NFKB1 +13 more
Innate lymphoid cells	Interferon-Stimulated Genes Inflammation	ALDOA, CRTAP, DAZAP2, DDX39B, EIF4B, GDI1, GNB2, GRINA +17 more	View in SCUBA
Lymphatic endothelial	NF-κB Autophagy Regulation Immune regulation	CLIC2, GABARAPL1, LGMN, NFKBIB, OSER1, PRRG4, RNF114, SQSTM1 +3 more	View in SCUBA
Monocytes	Non-canonical NF-κB Innate immunity	AMPD2, BCL3, BEST1, DENND5A, FAM20A, NFKB2, NOCT, TICAM1	View in SCUBA
Mucosal-associated invariant T cell	NF-κB Activation Inflammation	DUSP5, DUSP8, ELL2, GABARAPL1, IRF2BP2, MAFF, NAMPT, NFKB1 +8 more
Natural Killer cells	Circadian NF-κB Crosstalk Inflammation	DUSP8, IRF2BP2, ISCA1, MAP3K8, MED10, PER1, RHOH, SLC7A5	View in SCUBA
Neutrophils	NF-κB Inflammatory Transcription Inflammatory	BID, C9orf72, DENND5A, ELL2, ETF1, N4BP1, NFE2L2, NFKB1 +10 more

About the gene

Synonyms	REL-B
Chromosome	19: 45001461-45038192
Predicted location	Intracellular
Essential gene	No
Protein class	Cancer-related genes, Disease related genes, Human disease related genes, Plasma proteins, Predicted intracellular proteins, Transcription factors
Molecular function	Activator, DNA-binding, Repressor
Biological process	Biological rhythms, Transcription, Transcription regulation

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.

Human Protein Atlas · Open Targets · UniProt

Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.