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UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 6 (B3GNT6)

Target: B3GNT6
Molecular classification: Enzyme (Glycosyltransferase), Beta-1,3-N-acetylglucosaminyltransferase

Overview

UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 6 (B3GNT6) is a key glycosyltransferase enzyme responsible for synthesizing the core 3 structure of O-glycans by transferring N-acetylglucosamine to N-acetylgalactosamine-modified serine or threonine residues in glycoproteins. Found predominantly in gastrointestinal tissues, B3GNT6 plays an essential role in maintaining mucosal barrier integrity via the modification of mucin-type glycoproteins. Its expression is frequently downregulated in various cancers, particularly colorectal cancer, where low B3GNT6 correlates with poor prognosis, chromosomal instability, and increased proteasome activity. As such, B3GNT6 serves both as a biomarker and a potential therapeutic target for modulating glycosylation-dependent cellular functions in disease states.

Other names: Core 3 synthaseacetylgalactosaminyl-O-glycosyl-glycoprotein beta-1,3-N-acetylglucosaminyltransferaseBeta-1,3-N-acetylglucosaminyltransferase 6B3Gn-T6BGnT-6Beta3Gn-T6Beta-1,3-Gn-T6

Mechanism of action

Modulators would influence the enzymatic activity for core 3 O-glycan synthesis and thereby impact glycoprotein structure/function; Indirectly regulate signaling (KRAS/ERK, proteasome activity)

Biological functions

Biosynthesis of core 3 O-glycansModification of mucin-type glycoproteinsRegulation of cell adhesion and signalingMaintenance of gastrointestinal mucosal integrity

Disease associations

Cancer (colorectal, pancreatic, prostate, cholangiocarcinoma)Associated with chromosome instability (CIN) and KRAS mutation in colorectal cancerPossible involvement in neuropsychiatric disorders (e.g., childhood-onset schizophrenia)

Safety considerations

Therapeutic targeting could disrupt mucosal barrier functionAffect glycoprotein stabilityHave gastrointestinal side effects; details remain to be clarified in clinical studies

Interacting drugs

None directly approved or listed; however, inhibitors of the proteasome or pathways affected by B3GNT6 expression (e.g., KRAS/ERK signaling, O-glycosylation inhibitors) are of research interest

Biomarkers

Low expression of B3GNT6 as a marker for poor prognosis in colorectal cancerDownregulation linked to CIN, KRAS mutations, increased proteasome activity

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