RELB
Transcription factor RelB
Also known as: REL-B, RELB_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q01201
- Gene
- RELB
- Ensembl
- ENSG00000104856
- Chromosome
- 19
- Canonical length
- 579 aa
- Protein class
- Cancer-related genes, Disease related genes, Human disease related genes, Plasma proteins, Predicted intracellular proteins, Transcription factors
- Subcellular location
- Nucleoplasm,Cytosol
OverviewNCBI Gene
Enables RNA polymerase II cis-regulatory region sequence-specific DNA binding activity and protein kinase binding activity. Involved in lymphocyte differentiation and negative regulation of interferon-beta production. Located in several cellular components, including centrosome; chromatin; and nucleoplasm. Part of nucleus and transcription repressor complex. Implicated in breast cancer and immunodeficiency 53. Biomarker of breast cancer and transitional cell carcinoma. [provided by Alliance of Genome Resources, Jul 2025]
Canonical amino-acid sequenceUniProt
579 residues, UniProt reviewed canonical sequence.
>Q01201|RELB
1 MLRSGPASGP SVPTGRAMPS RRVARPPAAP ELGALGSPDL SSLSLAVSRS TDELEIIDEY
61 IKENGFGLDG GQPGPGEGLP RLVSRGAASL STVTLGPVAP PATPPPWGCP LGRLVSPAPG
121 PGPQPHLVIT EQPKQRGMRF RYECEGRSAG SILGESSTEA SKTLPAIELR DCGGLREVEV
181 TACLVWKDWP HRVHPHSLVG KDCTDGICRV RLRPHVSPRH SFNNLGIQCV RKKEIEAAIE
241 RKIQLGIDPY NAGSLKNHQE VDMNVVRICF QASYRDQQGQ MRRMDPVLSE PVYDKKSTNT
301 SELRICRINK ESGPCTGGEE LYLLCDKVQK EDISVVFSRA SWEGRADFSQ ADVHRQIAIV
361 FKTPPYEDLE IVEPVTVNVF LQRLTDGVCS EPLPFTYLPR DHDSYGVDKK RKRGMPDVLG
421 ELNSSDPHGI ESKRRKKKPA ILDHFLPNHG SGPFLPPSAL LPDPDFFSGT VSLPGLEPPG
481 GPDLLDDGFA YDPTAPTLFT MLDLLPPAPP HASAVVCSGG AGAVVGETPG PEPLTLDSYQ
541 APGPGDGGTA SLVGSNMFPN HYREAAFGGG LLSPGPEATLocalizationUniProt · AlphaFold · HPA
Whether an antibody against RELB can act on the native protein depends on physical access: surface and secreted proteins are reachable by circulating antibodies, intracellular proteins usually are not.
- Antibody reachability
- Intracellular
- Secreted
- No
- Transmembrane segments
- 0
- Mean surface accessibility (rSASA)
- 0.51
- Highest tissue expression
- 34 nTPM
Expression across tissuesHPA
Tissue
- bone marrow: 34 nTPM
- spleen: 25 nTPM
- lung: 21 nTPM
- kidney: 17 nTPM
- lymph node: 17 nTPM
- appendix: 16 nTPM
Single-cell type
- neutrophils: 625 nCPM
- enterocytes: 323 nCPM
- mast cells: 295 nCPM
- colonocytes: 206 nCPM
- monocytes: 197 nCPM
- pancreatic duct cells: 195 nCPM
Immune cell
- neutrophil: 16 nTPM
- memory B-cell: 9.2 nTPM
- naive B-cell: 7.7 nTPM
- classical monocyte: 5.2 nTPM
- plasmacytoid DC: 4.1 nTPM
- myeloid DC: 3.9 nTPM
Brain region
- medulla oblongata: 8.4 nTPM
- thalamus: 8.2 nTPM
- cerebral cortex: 6.7 nTPM
- white matter: 6.5 nTPM
- pons: 6.2 nTPM
- spinal cord: 5.7 nTPM
DiseaseUniProt · ClinVar · IEDB · PubMed
Four sources answering four different questions about RELB.
Disease | AllUniProt
Conditions RELB is implicated in, by any mechanism.
- Immunodeficiency 53 (IMD53) MIM:617585
Disease | GeneticClinVar
2 pathogenic / likely-pathogenic of 539 ClinVar records.
Conditions with pathogenic or likely-pathogenic variants.
- Immunodeficiency 53
Genetic constraint and essentialitygnomAD · DepMap
Does the body need this protein intact? Low LOEUF or a strong DepMap dependency means loss or blockade of the protein is likely to be felt.
- gnomAD LOEUF (loss-of-function intolerance)
- 0.26
- gnomAD pLI
- 0.99
- gnomAD missense Z
- 2.28
- DepMap mean gene effect
- 0.02
- DepMap dependency class
- selective
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 5% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- antigen processing and presentation
- canonical NF-kappaB signal transduction
- cellular response to osmotic stress
- circadian regulation of gene expression
- inflammatory response
- innate immune response
- lymphocyte differentiation
- myeloid dendritic cell differentiation
- negative regulation of DNA-templated transcription
- negative regulation of interferon-beta production
- non-canonical NF-kappaB signal transduction
- positive regulation of transcription by RNA polymerase II
- response to cytokine
- T-helper 1 cell differentiation
Molecular functions
- DNA-binding transcription factor activity, RNA polymerase II-specific
- identical protein binding
- protein kinase binding
- RNA polymerase II cis-regulatory region sequence-specific DNA binding
Cellular components
Protein domainsUniProt · Pfam · InterPro
- NF-kappa-B/Dorsal
- IPT domain
- p53-like transcription factor, DNA-binding domain superfamily
- Rel homology domain, DNA-binding domain
- Immunoglobulin-like fold
- Immunoglobulin E-set
- Rel homology domain, conserved site
- Rel homology dimerisation domain
- NFkappaB IPT domain
- Rel homology domain (RHD), DNA-binding domain superfamily
- Rel homology DNA-binding domain
- Rel homology dimerisation domain
- Transcription factor RelB, RHD domain, N-terminal
- RelB leucine zipper
- RelB transactivation domain
- RelB leucine zipper
- RelB transactivation domain
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of RELB in the human serome: UniProt-annotated complex subunits plus reported interactors. Each links to its own Seroatlas record.
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads RELB as an antibody target. Whether an autoantibody or antibody against RELB could matter depends on whether native RELB is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
RELB is annotated as predominantly intracellular. Intracellular proteins are common autoantibody markers, becoming visible to the immune system after cell injury or altered processing, but are usually markers of disease rather than direct drivers.
Annotation status
The present source text does not explicitly label RELB as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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