RELB

Transcription factor RelB is a protein that in humans is encoded by the RELB gene.^[5]

RELB
Available structures PDB Ortholog search: PDBe RCSB List of PDB id codes 1ZK9, 1ZKA, 2V2T, 3DO7, 3JSS, 3JUZ, 3JV0, 3JV4, 3JV6, 4JGM, 4JHB
Identifiers
Aliases	RELB, I-REL, IREL, REL-B, RELB proto-oncogene, NF-kB subunit, IMD53
External IDs	OMIM: 604758; MGI: 103289; HomoloGene: 4747; GeneCards: RELB; OMA:RELB - orthologs
Gene location (Human) Chr. Chromosome 19 (human)[1] Band 19q13.32 Start 45,001,449 bp[1] End 45,038,198 bp[1]
Gene location (Mouse) Chr. Chromosome 7 (mouse)[2] Band 7 A3|7 9.93 cM Start 19,340,142 bp[2] End 19,363,363 bp[2]
RNA expression pattern Bgee Human Mouse (ortholog) Top expressed in granulocyte mucosa of transverse colon cartilage tissue monocyte spleen olfactory zone of nasal mucosa blood upper lobe of left lung stromal cell of endometrium muscle of thigh Top expressed in mesenteric lymph nodes jejunum intestinal villus granulocyte spleen duodenum lactiferous gland colon left colon thymus More reference expression data BioGPS More reference expression data
Gene ontology Molecular function DNA binding RNA polymerase II transcription regulatory region sequence-specific DNA binding transcription corepressor activity DNA-binding transcription factor activity chromatin binding protein binding protein kinase binding identical protein binding DNA-binding transcription factor activity, RNA polymerase II-specific RNA polymerase II cis-regulatory region sequence-specific DNA binding Cellular component I-kappaB/NF-kappaB complex nucleoplasm microtubule organizing center cytoskeleton nucleus cytoplasm cytosol centrosome protein-containing complex transcription repressor complex Biological process response to cytokine antigen processing and presentation regulation of transcription, DNA-templated rhythmic process regulation of transcription by RNA polymerase II myeloid dendritic cell differentiation stimulatory C-type lectin receptor signaling pathway negative regulation of transcription by RNA polymerase II T-helper 1 cell differentiation negative regulation of interferon-beta production circadian regulation of gene expression transcription, DNA-templated cellular response to osmotic stress positive regulation of gene expression NIK/NF-kappaB signaling T-helper 1 type immune response inflammatory response negative regulation of transcription, DNA-templated I-kappaB kinase/NF-kappaB signaling positive regulation of transcription by RNA polymerase II innate immune response lymphocyte differentiation Sources:Amigo / QuickGO
Orthologs Species Human Mouse Entrez 5971 19698 Ensembl ENSG00000104856 ENSMUSG00000002983 UniProt Q01201 Q04863 RefSeq (mRNA) NM_006509 NM_001290457 NM_009046 RefSeq (protein) NP_006500 NP_001277386 NP_033072 Location (UCSC) Chr 19: 45 – 45.04 Mb Chr 7: 19.34 – 19.36 Mb PubMed search [3] [4]
Wikidata
View/Edit Human View/Edit Mouse

Interactions

RELB has been shown to interact with NFKB2,^[6][7] NFKB1,^[6] and C22orf25.^[8]

Activation and function

In resting cells, RelB is sequestered by the NF-κB precursor protein p100 in the cytoplasm. A select set of TNF-R superfamily members, including lymphotoxin β-receptor (LTβR), BAFF-R, CD40 and RANK, activate the non-canonical NF-κB pathway. In this pathway, NIK stimulates the processing of p100 into p52, which in association with RelB appears in the nucleus as RelB:p52 NF-κB heterodimers. RelB:p52 activates the expression homeostatic lymphokines,^[9] which instruct lymphoid organogenesis and determine the trafficking of naive lymphocytes in the secondary lymphoid organs.

Recent studies has suggested that the functional non-canonical NF-κB pathway is modulated by canonical NF-κB signalling. For example, syntheses of the constituents of the non-canonical pathway, viz RelB and p52, are controlled by canonical IKK2-IκB-RelA:p50 signalling.^[10] Moreover, generation of canonical and non-canonical dimers, viz RelA:p50 and RelB:p52, within the cellular milieu are mechanistically interlinked. These analyses suggest that an integrated NF-κB system network underlies activation of both RelA and RelB containing dimer and that a malfunctioning canonical pathway will lead to an aberrant cellular response also through the non-canonical pathway.

Most intriguingly, a recent study identified that TNF-induced canonical signalling subverts non-canonical RelB:p52 activity in the inflamed lymphoid tissues limiting lymphocyte ingress.^[11] Mechanistically, TNF inactivated NIK in LTβR‐stimulated cells and induced the synthesis of Nfkb2 mRNA encoding p100; these together potently accumulated unprocessed p100, which attenuated the RelB activity. A role of p100/Nfkb2 in dictating lymphocyte ingress in the inflamed lymphoid tissue may have broad physiological implications.

See also

• NF-κB