BCL3
B-cell lymphoma 3 protein
Also known as: BCL3_HUMAN, BCL4, D19S37
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- P20749
- Gene
- BCL3
- Ensembl
- ENSG00000069399
- Chromosome
- 19
- Canonical length
- 454 aa
- Protein class
- Cancer-related genes, Disease related genes, Plasma proteins, Predicted intracellular proteins, Transcription factors
- Subcellular location
- Nucleoplasm,Vesicles,Midbody,Basal body,Cytosol
- Quaternary structure
- Homodimer
OverviewNCBI Gene
This gene is a proto-oncogene candidate. It is identified by its translocation into the immunoglobulin alpha-locus in some cases of B-cell leukemia. The protein encoded by this gene contains seven ankyrin repeats, which are most closely related to those found in I kappa B proteins. This protein functions as a transcriptional co-activator that activates through its association with NF-kappa B homodimers. The expression of this gene can be induced by NF-kappa B, which forms a part of the autoregulatory loop that controls the nuclear residence of p50 NF-kappa B. [provided by RefSeq, Jul 2008]
Canonical amino-acid sequenceUniProt
454 residues, UniProt reviewed canonical sequence.
>P20749|BCL3
1 MPRCPAGAMD EGPVDLRTRP KAAGLPGAAL PLRKRPLRAP SPEPAAPRGA AGLVVPLDPL
61 RGGCDLPAVP GPPHGLARPE ALYYPGALLP LYPTRAMGSP FPLVNLPTPL YPMMCPMEHP
121 LSADIAMATR ADEDGDTPLH IAVVQGNLPA VHRLVNLFQQ GGRELDIYNN LRQTPLHLAV
181 ITTLPSVVRL LVTAGASPMA LDRHGQTAAH LACEHRSPTC LRALLDSAAP GTLDLEARNY
241 DGLTALHVAV NTECQETVQL LLERGADIDA VDIKSGRSPL IHAVENNSLS MVQLLLQHGA
301 NVNAQMYSGS SALHSASGRG LLPLVRTLVR SGADSSLKNC HNDTPLMVAR SRRVIDILRG
361 KATRPASTSQ PDPSPDRSAN TSPESSSRLS SNGLLSASPS SSPSQSPPRD PPGFPMAPPN
421 FFLPSPSPPA FLPFAGVLRG PGRPVPPSPA PGGSLocalizationUniProt · AlphaFold · HPA
Whether an antibody against BCL3 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)
- 0.47
- Highest tissue expression
- 169 nTPM
Expression across tissuesHPA
Tissue
- liver: 169 nTPM
- lung: 95 nTPM
- esophagus: 75 nTPM
- adipose tissue: 70 nTPM
- spleen: 63 nTPM
- bone marrow: 51 nTPM
Single-cell type
- neutrophils: 368 nCPM
- breast hormone-responsive cells: 163 nCPM
- breast secretory cells: 131 nCPM
- esophageal apical cells: 118 nCPM
- monocytes: 110 nCPM
- urothelial cells: 101 nCPM
Immune cell
- neutrophil: 20 nTPM
- eosinophil: 5.5 nTPM
- plasmacytoid DC: 3.1 nTPM
- classical monocyte: 2.7 nTPM
- myeloid DC: 2.6 nTPM
- NK-cell: 2.3 nTPM
Brain region
- medulla oblongata: 15 nTPM
- thalamus: 9.6 nTPM
- pons: 8.5 nTPM
- spinal cord: 8.4 nTPM
- choroid plexus: 8.1 nTPM
- midbrain: 7.8 nTPM
DiseaseUniProt · ClinVar · IEDB · PubMed
Four sources answering four different questions about BCL3.
Disease | ImmuneIEDB
Conditions an epitope on BCL3 was assayed in.
- nodular malignant melanoma T cell
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)
- 0.22
- gnomAD pLI
- 0.99
- gnomAD missense Z
- 2.27
- DepMap mean gene effect
- 0.07
- 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
- antimicrobial humoral response
- canonical NF-kappaB signal transduction
- defense response to bacterium
- defense response to protozoan
- DNA damage response
- DNA damage response, signal transduction by p53 class mediator
- extracellular matrix organization
- follicular dendritic cell differentiation
- germinal center formation
- humoral immune response mediated by circulating immunoglobulin
- intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator
- marginal zone B cell differentiation
- negative regulation of apoptotic process
- negative regulation of DNA-templated transcription
- negative regulation of interleukin-8 production
- negative regulation of NF-kappaB transcription factor activity
- negative regulation of receptor signaling pathway via JAK-STAT
- negative regulation of T cell apoptotic process
- negative regulation of tumor necrosis factor production
- positive regulation of DNA-templated transcription
- positive regulation of interleukin-10 production
- positive regulation of transcription by RNA polymerase II
- positive regulation of translation
- positive regulation of type II interferon production
- protein import into nucleus
- regulation of apoptotic process
- regulation of DNA binding
- regulation of non-canonical NF-kappaB signal transduction
- response to UV-C
- response to virus
- spleen development
- T cell apoptotic process
- T-helper 1 type immune response
- T-helper 2 cell differentiation
Molecular functions
- DNA-binding transcription factor binding
- histone deacetylase binding
- protein-macromolecule adaptor activity
- transcription coactivator activity
- transcription corepressor activity
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of BCL3 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 BCL3 as an antibody target. Whether an autoantibody or antibody against BCL3 could matter depends on whether native BCL3 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
BCL3 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 BCL3 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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