B3GNT8
UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 8
Also known as: B3GALT7, B3GN8_HUMAN, beta3Gn-T8, BGALT15
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q7Z7M8
- Gene
- B3GNT8
- Ensembl
- ENSG00000177191
- Chromosome
- 19
- Canonical length
- 397 aa
- Protein class
- Metabolic proteins, Predicted intracellular proteins
- Secretome location
- Intracellular and membrane
OverviewNCBI Gene
Enables protein N-acetylglucosaminyltransferase activity. Involved in poly-N-acetyllactosamine biosynthetic process. Located in extracellular exosome. [provided by Alliance of Genome Resources, Jul 2025]
Canonical amino-acid sequenceUniProt
397 residues, UniProt reviewed canonical sequence.
>Q7Z7M8|B3GNT8
1 MRCPKCLLCL SALLTLLGLK VYIEWTSESR LSKAYPSPRG TPPSPTPANP EPTLPANLST
61 RLGQTIPLPF AYWNQQQWRL GSLPSGDSTE TGGCQAWGAA AATEIPDFAS YPKDLRRFLL
121 SAACRSFPQW LPGGGGSQVS SCSDTDVPYL LLAVKSEPGR FAERQAVRET WGSPAPGIRL
181 LFLLGSPVGE AGPDLDSLVA WESRRYSDLL LWDFLDVPFN QTLKDLLLLA WLGRHCPTVS
241 FVLRAQDDAF VHTPALLAHL RALPPASARS LYLGEVFTQA MPLRKPGGPF YVPESFFEGG
301 YPAYASGGGY VIAGRLAPWL LRAAARVAPF PFEDVYTGLC IRALGLVPQA HPGFLTAWPA
361 DRTADHCAFR NLLLVRPLGP QASIRLWKQL QDPRLQCLocalizationUniProt · AlphaFold · HPA
Whether an antibody against B3GNT8 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
- Other membrane
- Secreted
- No
- Transmembrane segments
- 1
- Mean surface accessibility (rSASA)
- 0.28
- Highest tissue expression
- 19 nTPM
Expression across tissuesHPA
Tissue
- duodenum: 19 nTPM
- small intestine: 18 nTPM
- esophagus: 12 nTPM
- colon: 11 nTPM
- lung: 7 nTPM
- bone marrow: 4.5 nTPM
Single-cell type
- esophageal apical cells: 659 nCPM
- esophageal suprabasal cells: 102 nCPM
- neutrophils: 74 nCPM
- enterocytes: 66 nCPM
- colonocytes: 53 nCPM
- alveolar cells type 2: 48 nCPM
Immune cell
- neutrophil: 198 nTPM
- eosinophil: 147 nTPM
- basophil: 118 nTPM
- MAIT T-cell: 35 nTPM
- non-classical monocyte: 33 nTPM
- classical monocyte: 20 nTPM
Brain region
- cerebellum: 4.1 nTPM
- pons: 3 nTPM
- white matter: 3 nTPM
- medulla oblongata: 2.7 nTPM
- basal ganglia: 2.5 nTPM
- cerebral cortex: 2.5 nTPM
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)
- 1.54
- gnomAD pLI
- 0
- gnomAD missense Z
- 0.22
- DepMap mean gene effect
- 0.06
- DepMap dependency class
- none
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 4% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
Molecular functions
- N-acetyllactosaminide beta-1,3-N-acetylglucosaminyltransferase activity
- protein N-acetylglucosaminyltransferase activity
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of B3GNT8 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 B3GNT8 as an antibody target. Whether an autoantibody or antibody against B3GNT8 could matter depends on whether native B3GNT8 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
B3GNT8 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 B3GNT8 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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