Affinage

POFUT2

GDP-fucose protein O-fucosyltransferase 2 · UniProt Q9Y2G5

Length
429 aa
Mass
50.0 kDa
Annotated
2026-06-10
46 papers in source corpus 19 papers cited in narrative 19 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

POFUT2 is an ER-resident GT-B fold glycosyltransferase that O-fucosylates serine/threonine residues within thrombospondin type 1 repeats (TSRs), functioning as a noncanonical ER quality-control factor that promotes folding and efficient secretion of TSR-containing proteins (PMID:22588082, PMID:25544610). It recognizes the three-dimensional fold of a small part of the folded TSR rather than primary sequence, requires properly disulfide-bonded TSRs containing a minimal C-X-X-S/T-C consensus, and transfers fucose via an inverting SN2-like mechanism in which a solvent-exposed active site and a network of water molecules assist GDP release and proton transfer to a catalytic base (PMID:22588082, PMID:26854667, PMID:36260536). The added O-fucose is elongated by B3GLCT to a Glcβ1-3Fuc disaccharide, which contacts residues proximal to the fucosylation site and protects nearby disulfide bonds, stabilizing the TSR fold (PMID:35597280, PMID:16899492). Through this activity POFUT2 is required for secretion of numerous TSR-bearing substrates including ADAMTS13, ADAMTS-like-1/punctin-1, CCN1, ADAMTS9, and ADAMTSL2, with POFUT2 affecting all tested targets while B3GLCT affects only a subset (PMID:25544610, PMID:17395589, PMID:17395588, PMID:27297885, PMID:32913123). In vivo, POFUT2 controls extracellular matrix–dependent growth factor signaling: its loss causes embryonic lethality with aberrant Nodal, BMP4, Fgf8, and Wnt3 signaling during gastrulation specifically through failure to secrete ADAMTS9 (PMID:20637190, PMID:27297885), and conditional deletion in limb mesenchyme produces bone shortening with fibrillin-2 accumulation and dysregulated BMP, IHH, and TGF-β signaling (PMID:35167946). Substrate dependence on POFUT2 is context-specific, as C-mannosylation can compensate to stabilize TSRs and support THBS1 trafficking in platelets (PMID:36721988). A loss-of-O-fucosylation mutation (S641L) in ADAMTSL2 links impaired POFUT2 modification to geleophysic dysplasia (PMID:32913123).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2004 Medium

    Initial characterization established POFUT2 (C21orf80) as a candidate O-fucosyltransferase with a developmental role, framing the question of what it modifies and where it acts.

    Evidence Tagged protein localization and C. elegans ortholog (pad-2) RNAi/overexpression phenotypes

    PMID:15233996

    Open questions at the time
    • Catalytic activity and substrate not yet demonstrated biochemically
    • Localization based on overexpressed tagged protein
  2. 2006 High

    Defined the downstream glycan-elaboration step, showing POFUT2-added fucose must precede B3GLCT-mediated glucose addition to form Glcβ1-3Fuc.

    Evidence In vitro sequential glucosyltransferase reconstitution with recombinant enzymes and TLC/glycosidase analysis

    PMID:16899492

    Open questions at the time
    • Functional consequence of disaccharide for substrate fate not yet addressed
    • Did not establish substrate range of either enzyme
  3. 2007 High

    Established that POFUT2-dependent O-fucosylation of TSRs is functionally required for efficient secretion of native substrates ADAMTS13 and ADAMTS-like-1.

    Evidence siRNA knockdown, site-directed mutagenesis, metabolic labeling, MS, and rescue in GDP-fucose-deficient cells

    PMID:17395588 PMID:17395589

    Open questions at the time
    • Molecular mechanism linking fucosylation to secretion unresolved
    • Generality across the TSR-containing proteome untested
  4. 2010 High

    Connected POFUT2 enzymatic activity to a whole-organism phenotype, showing it modulates ECM-dependent growth factor signaling during gastrulation.

    Evidence Two independent gene-trap mouse knockouts with immunofluorescence, in situ hybridization, and teratoma assays

    PMID:20637190

    Open questions at the time
    • Which TSR substrate mediates the phenotype not identified
    • Direct biochemical link to signaling ligands not shown
  5. 2012 High

    Resolved the structural and kinetic basis of substrate recognition, showing specificity is encoded in the folded 3D structure of the TSR rather than sequence.

    Evidence X-ray crystallography and steady-state kinetics of wild-type/mutant POFUT2 with mini-TSR substrates

    PMID:22588082

    Open questions at the time
    • Enzyme-substrate complex geometry not yet captured
    • Catalytic mechanism not defined
  6. 2014 High

    Defined POFUT2 as a noncanonical ER quality-control factor acting co-translationally to recognize and stabilize folded TSRs, distinguishing its broad requirement from B3GLCT's subset effect.

    Evidence Mass spectrometry of secreted vs ER TSRs, in vitro refolding assays under redox conditions, and cell-based secretion assays

    PMID:25544610

    Open questions at the time
    • Atomic mechanism of fold stabilization not yet structurally defined
    • Interplay with canonical ER chaperones unaddressed
  7. 2016 High

    Captured the enzyme-substrate complex and catalytic preference, demonstrating an inverting mechanism with a catalytic base, water-mediated contacts, and Thr-over-Ser preference for folded TSRs.

    Evidence Crystal structure of C. elegans POFUT2-GDP-human TSR1, site-directed mutagenesis, and MD simulations

    PMID:26854667

    Open questions at the time
    • Detailed chemistry of proton transfer/leaving-group departure not fully resolved
    • Group-2 TSR recognition not yet structurally examined
  8. 2016 High

    Identified ADAMTS9 as the specific substrate whose loss of secretion drives the gastrulation defect, establishing in vivo epistasis.

    Evidence Germline and conditional Pofut2/Adamts9 mouse knockouts with conditional rescue plus CRISPR knockout secretion assays in HEK293T

    PMID:27297885

    Open questions at the time
    • Whether other TSR substrates contribute in other tissues unknown
    • Mechanism by which ADAMTS9 loss alters signaling not detailed
  9. 2020 High

    Extended the substrate set and linked POFUT2-dependent secretion failure to human disease via geleophysic dysplasia ADAMTSL2 mutations.

    Evidence MS glycan mapping, CRISPR POFUT2-/-/B3GLCT-/- cells, secretion assays, and mutagenesis of TSR fucosylation sites

    PMID:32913123

    Open questions at the time
    • Whether all geleophysic dysplasia alleles act through O-fucosylation loss unresolved
    • In vivo validation of ADAMTSL2 mechanism not provided
  10. 2022 High

    Provided atomic and quantum-chemical resolution of catalysis and of how the Glc-Fuc disaccharide stabilizes the TSR by protecting a nearby disulfide bond.

    Evidence X-ray crystallography, NMR, QM/MM calculations, MD simulations, and in vitro unfolding assays with mutagenesis

    PMID:35597280 PMID:36260536

    Open questions at the time
    • Generalizability of disaccharide protection across all TSR types untested
    • Kinetic contribution of each catalytic water not quantified
  11. 2022 High

    Showed substrate dependence on POFUT2 is cell-type specific and extends to bone development through ECM remodeling and altered morphogen signaling.

    Evidence Prrx1-Cre conditional Pofut2 knockout with FBN2 accumulation, signaling analysis, and cell-based secretion assays

    PMID:35167946

    Open questions at the time
    • Direct FBN2 fucosylation status not established
    • Causal chain from FBN2 accumulation to signaling changes incomplete
  12. 2023 Medium

    Defined an exception to the secretion-requirement rule, showing C-mannosylation can compensate for loss of O-fucosylation in stabilizing TSRs in a specific context.

    Evidence CRISPR Pofut2/B3glct mouse knockouts with platelet fractionation and MS glycan analysis

    PMID:36721988

    Open questions at the time
    • Extent of C-mannosylation compensation across other substrates unknown
    • Mechanism of redundancy not biochemically dissected
  13. 2025 Low

    Reported a potential noncanonical substrate and disease context, proposing POFUT2 fucosylates JUP to drive VEGFA-dependent angiogenesis in colorectal cancer.

    Evidence Flag-IP/MS, co-IP, western blot, and angiogenesis assays in colorectal cancer cells

    PMID:41583504

    Open questions at the time
    • No in vitro fucosylation assay confirming JUP as a direct catalytic substrate
    • JUP lacks the canonical TSR substrate context; mechanism of fucosylation-dependent upregulation unclear
  14. 2025 Medium

    Placed POFUT2 within inflammatory transcriptional circuits relevant to parturition, with NF-κB co-regulating POFUT2 and ADAMTS9 to drive ECM degradation.

    Evidence ChIP, luciferase promoter assays, fetal membrane explants, and intra-amniotic injection mouse model

    PMID:40057799

    Open questions at the time
    • Direct contribution of POFUT2 transcriptional induction vs ADAMTS9 induction not separated
    • Single lab without independent replication
  15. 2026 Medium

    Identified hormonal transcriptional control of POFUT2 via the ESR2/SP1 complex linked to trophoblast syncytialization.

    Evidence ChIP and co-IP of ESR2/SP1 at the POFUT2 promoter plus in vitro syncytialization assay

    PMID:41672297

    Open questions at the time
    • Downstream TSR substrate mediating syncytialization not identified
    • In vivo relevance of the regulatory axis not established

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how POFUT2 activity is selectively required for some substrates and tissues but dispensable in others, and whether non-TSR substrates such as JUP represent a genuine catalytic activity.
  • No unified model of context-dependent substrate dependence
  • Direct fucosylation of proposed non-TSR substrates not biochemically confirmed
  • Tissue-specific compensation mechanisms incompletely mapped

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016740 transferase activity 4 GO:0140096 catalytic activity, acting on a protein 4 GO:0016787 hydrolase activity 2
Localization
GO:0005783 endoplasmic reticulum 2 GO:0005794 Golgi apparatus 1
Pathway
R-HSA-1266738 Developmental Biology 3 R-HSA-1474244 Extracellular matrix organization 3 R-HSA-392499 Metabolism of proteins 3
Partners
ADAMTS13ADAMTS9ADAMTSL1ADAMTSL2B3GLCTCCN1

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2012 Crystal structures of human POFUT2 reveal a variation of the classical GT-B fold. Structural and kinetic analysis of wild-type and mutant POFUT2 identified sugar donor (GDP-fucose) and TSR acceptor binding sites. Using an artificial mini-TSR substrate, specificity was shown to be encoded not primarily in TSR protein sequence but in the unusual 3D structure of a small part of the folded TSR. X-ray crystallography, steady-state kinetic measurements of wild-type and mutant POFUT2 and TSR substrates The EMBO journal High 22588082
2016 Crystal structure of C. elegans POFUT2 in complex with GDP and human TSR1 shows an inverting mechanism for fucose transfer assisted by a catalytic base, with nearly half of TSR1 embraced by POFUT2. A small number of direct protein-protein contacts and a large network of water-mediated interactions maintain the complex. Site-directed mutagenesis demonstrated that POFUT2 fucosylates threonine preferentially over serine and requires folded TSRs containing the minimal consensus sequence C-X-X-S/T-C. X-ray crystallography (fusion protein approach), site-directed mutagenesis, atomic-level MD simulations Nature chemical biology High 26854667
2022 X-ray crystallography and NMR evidence, combined with MD simulations, demonstrate that the Glucose-Fucose disaccharide added by POFUT2 (and B3GLCT) interacts with specific amino acids in TSR3 of thrombospondin-1 proximal to the O-fucosylation site, protecting a nearby disulfide bond. Mutation of these interacting amino acids reduces the stabilizing effect of the sugars in vitro. X-ray crystallography, NMR, molecular dynamics simulations, in vitro unfolding assays with mutagenesis The Journal of biological chemistry High 35597280
2022 QM/MM computational studies using human POFUT2 as a model demonstrate that POFUT2 follows a classical SN2 (inverting) reaction mechanism in which water molecules facilitate release of the GDP leaving group and mediate H transfer from the acceptor nucleophile (Thr/Ser) to the catalytic base as the last catalytic event. This is corroborated by a new X-ray structure of C. elegans POFUT2 complexed with a group-2 TSR, showing the active site is highly solvent-exposed. X-ray crystallography, QM/MM calculations Angewandte Chemie (International ed. in English) High 36260536
2014 POFUT2 (and downstream B3GLCT) mediate a noncanonical ER quality-control mechanism: O-glycosylation occurs co-translationally as TSRs fold; mass spectrometry shows TSRs from mature secreted protein are stoichiometrically modified while TSRs still folding in the ER are partially modified. In vitro refolding assays show POFUT2 recognizes, glycosylates, and stabilizes the folded form of TSRs, accelerating net folding. POFUT2 is required for secretion of all TSR-containing targets tested, whereas B3GLCT affects only a subset. Mass spectrometry, in vitro unfolding/refolding assays under redox conditions, cell-based secretion assays Current biology : CB High 25544610
2007 POFUT2 adds O-fucose to serines/threonines within TSR consensus sequences of ADAMTS13. siRNA knockdown of POFUT2 decreased secretion of ADAMTS13. Mutation of individual O-fucosylation sites on ADAMTS13 TSRs reduced secretion, and mutation of multiple sites dramatically reduced secretion regardless of which sites were mutated. Expression in GDP-fucose-deficient cells also reduced secretion, establishing that POFUT2-dependent O-fucosylation is required for efficient ADAMTS13 secretion. siRNA knockdown, site-directed mutagenesis, metabolic labeling with [3H]fucose, mass spectrometry, secretion assays in GDP-fucose-deficient cell lines The Journal of biological chemistry High 17395589
2007 POFUT2-dependent O-fucosylation of TSR2, TSR3, and TSR4 of ADAMTS-like-1/punctin-1 is required for efficient secretion: mutation of O-fucosylation sites reduced secreted punctin-1 levels, and expression in Lec-13 GDP-fucose-deficient cells substantially decreased secretion, which was restored by exogenous L-fucose. Mass spectrometry, site-directed mutagenesis, metabolic labeling, secretion assays in GDP-fucose-deficient cells The Journal of biological chemistry High 17395588
2010 Mouse Pofut2 specifically adds O-fucose to TSRs; knockout via two gene-trap alleles causes embryonic lethality with failure to restrict epithelial-to-mesenchymal transition in the primitive streak, abnormal mesoderm patterning, loss of epiblast pluripotency, and mislocalization of definitive endoderm. Nodal, BMP4, Fgf8, and Wnt3 signaling were markedly elevated and expanded in Pofut2 mutants, indicating O-fucosylation of TSR-containing ECM proteins modulates growth factor signaling during gastrulation. Gene-trap mouse knockout (two independent alleles), immunofluorescence, in situ hybridization, teratoma formation assay Developmental biology High 20637190
2016 Gastrulation defects in Pofut2-null mouse embryos result specifically from loss of O-fucosylation of ADAMTS9: Pofut2 and Adamts9 knockouts share disorganized epithelia and blocked mesoderm formation phenotypes; CRISPR/Cas9 knockout of POFUT2 in HEK293T cells blocked secretion of ADAMTS9; conditional deletion of either Pofut2 or Adamts9 in the epiblast rescued gastrulation defects. This establishes epistasis between POFUT2 and ADAMTS9 in gastrulation. Mouse knockout (Pofut2 and Adamts9 conditional and germline), Cre-mediated conditional deletion, CRISPR/Cas9 knockout in HEK293T cells, secretion assays, in situ hybridization Developmental biology High 27297885
2006 B3GLCT (beta3Glc-T) is an ER-localized glucosyltransferase that elongates the O-fucose on TSR domains added by POFUT2: the TSR domain must first be fucosylated by POFUT2 before it becomes a substrate for B3GLCT, which then adds glucose in a beta1,3 linkage to produce Glcbeta1-3Fuc. B3GLCT retention in the ER is mediated by a C-terminal KDEL-like 'REEL' sequence. In vitro glucosyltransferase assay with recombinant enzymes, TLC, beta-glucosidase/exo-glucanase digestion, immunostaining Glycobiology High 16899492
2015 POFUT2 O-fucosylates CCN1 at Thr242 within its TSR1 domain (confirmed by mass spectrometry); knockdown of POFUT2 decreased secreted and cell-surface levels of CCN1, establishing that POFUT2-dependent O-fucosylation at this site is required for efficient CCN1 secretion. Mass spectrometry, siRNA knockdown, cell surface localization and secretion assays FEBS letters Medium 26424659
2020 POFUT2 O-fucosylates six of seven TSRs in ADAMTSL2 at high stoichiometry (confirmed by MS). Loss of POFUT2 (POFUT2-/- cells) but not B3GLCT blocked ADAMTSL2 secretion. Two geleophysic dysplasia-causing mutations in ADAMTSL2 TSRs (S641L in TSR3, G817R in TSR6) significantly reduced secretion, and S641L eliminated O-fucosylation of TSR3, providing a mechanistic link between loss of O-fucosylation and disease pathology. Mass spectrometry, CRISPR/Cas9 knockout cell lines (POFUT2-/-, B3GLCT-/-), secretion assays, site-directed mutagenesis The Journal of biological chemistry High 32913123
2017 O-glycosylation of EGF repeats by POFUT1 and POGLUT1 stabilizes individual EGF repeats against unfolding in an additive manner, regulating Notch trafficking. Crystal structure of a single EGF repeat modified by an O-glucose trisaccharide at 2.2 Å resolution shows the glycan filling a surface groove with multiple contacts, providing a structural basis for stabilization. (Note: this finding concerns POFUT1/POGLUT1 acting on EGF repeats, not POFUT2 acting on TSRs; included only to the extent it contextualizes POFUT2's parallel role demonstrated in the same paper.) In vitro unfolding assays, cell surface expression assays in HEK293T cells, X-ray crystallography The Journal of biological chemistry Low 28729422
2022 Conditional knockout of Pofut2 in limb mesenchyme (Prrx1-Cre) caused significant limb and long bone shortening with stiff joints, accompanied by accumulation of fibrillin 2 (FBN2), decreased BMP and IHH signaling, and increased TGF-β signaling in vivo. This indicates that O-fucosylation by POFUT2 is required for ECM remodeling and signaling during bone development and that its impact on substrate secretion is cell-type specific. Conditional mouse knockout (Prrx1-Cre), in vitro secretion assays in POFUT2-null HEK293T cells, immunofluorescence, signaling pathway analysis Matrix biology : journal of the International Society for Matrix Biology High 35167946
2023 O-fucosylation by POFUT2 is dispensable for trafficking of endogenous THBS1 to platelet secretory granules: CRISPR/Cas9-mediated knockout of Pofut2 or B3glct in mice did not reduce THBS1 trafficking to platelets. All three THBS1 TSRs from platelets were highly C-mannosylated, suggesting that C-mannosylation can compensate for loss of O-fucosylation in stabilizing TSRs in this context. CRISPR/Cas9 mouse knockout of Pofut2 and B3glct, platelet fractionation, mass spectrometry for glycan analysis Glycobiology Medium 36721988
2004 C21orf80 (alias for POFUT2) encodes a protein with potential O-fucosyltransferase activity. Transient expression of tagged C21orf80 proteins in cells shows primary intracellular localization in the Golgi apparatus. Its C. elegans ortholog pad-2 is required for normal embryonic morphogenesis (pad-2 RNAi causes failure of normal morphogenesis) and elevated pad-2 dosage causes body malformations and abnormal neuronal development. Tagged protein expression and immunolocalization, C. elegans RNAi, transgenic overexpression Genomics Medium 15233996
2025 POFUT2 interacts with and fucosylates Junction Plakoglobin (JUP) in colorectal cancer cells, upregulating JUP protein expression and subsequently increasing VEGFA levels to promote angiogenesis. Flag-immunoprecipitation combined with mass spectrometry identified JUP as a POFUT2-interacting protein; co-immunoprecipitation and western blot confirmed the POFUT2–JUP interaction and fucosylation-dependent JUP upregulation. Flag-immunoprecipitation/mass spectrometry, co-immunoprecipitation, western blot, angiogenesis assays, immunohistochemistry International journal of medical sciences Low 41583504
2026 Estradiol upregulates poFUT2 expression via the ESR2/SP1 transcription factor complex: chromatin immunoprecipitation and co-immunoprecipitation assays showed that SP1 participates in ESR2-mediated binding to the poFUT2 promoter. Elevated poFUT2 promotes trophoblast cell fusion/syncytialization in vitro. Chromatin immunoprecipitation, co-immunoprecipitation, in vitro syncytialization assay, immunohistochemistry Molecular and cellular endocrinology Medium 41672297
2025 IL-1β activates NF-κB, which binds to the promoters of both ADAMTS9 and POFUT2 (shown by ChIP and luciferase assays), upregulating their expression; POFUT2-dependent O-fucosylation then promotes ADAMTS9 secretion, leading to versican ECM degradation and fetal membrane weakening. Chromatin immunoprecipitation, luciferase promoter assay, ELISA, fetal membrane explants, murine intra-amniotic injection model Cell communication and signaling : CCS Medium 40057799

Source papers

Stage 0 corpus · 46 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2000 Collagen XVIII, containing an endogenous inhibitor of angiogenesis and tumor growth, plays a critical role in the maintenance of retinal structure and in neural tube closure (Knobloch syndrome). Human molecular genetics 221 10942434
2017 O-Glycosylation modulates the stability of epidermal growth factor-like repeats and thereby regulates Notch trafficking. The Journal of biological chemistry 95 28729422
2007 O-fucosylation is required for ADAMTS13 secretion. The Journal of biological chemistry 87 17395589
2011 Structural insights into the mechanism of protein O-fucosylation. PloS one 85 21966509
2014 Peters plus syndrome mutations disrupt a noncanonical ER quality-control mechanism. Current biology : CB 73 25544610
2010 O-fucosylation of thrombospondin type 1 repeats restricts epithelial to mesenchymal transition (EMT) and maintains epiblast pluripotency during mouse gastrulation. Developmental biology 69 20637190
2007 O-fucosylation of thrombospondin type 1 repeats in ADAMTS-like-1/punctin-1 regulates secretion: implications for the ADAMTS superfamily. The Journal of biological chemistry 66 17395588
2006 Molecular cloning and characterization of a novel human beta1,3-glucosyltransferase, which is localized at the endoplasmic reticulum and glucosylates O-linked fucosylglycan on thrombospondin type 1 repeat domain. Glycobiology 63 16899492
2012 Structure of human POFUT2: insights into thrombospondin type 1 repeat fold and O-fucosylation. The EMBO journal 60 22588082
2014 Novel roles for O-linked glycans in protein folding. Glycoconjugate journal 59 25186198
2016 A proactive role of water molecules in acceptor recognition by protein O-fucosyltransferase 2. Nature chemical biology 57 26854667
2003 A new superfamily of protein-O-fucosyltransferases, alpha2-fucosyltransferases, and alpha6-fucosyltransferases: phylogeny and identification of conserved peptide motifs. Glycobiology 56 12966037
2017 Protein O-fucosylation in Plasmodium falciparum ensures efficient infection of mosquito and vertebrate hosts. Nature communications 51 28916755
2016 Genetic and biochemical evidence that gastrulation defects in Pofut2 mutants result from defects in ADAMTS9 secretion. Developmental biology 39 27297885
2018 Fucosylation genes as circulating biomarkers for lung cancer. Journal of cancer research and clinical oncology 33 30101373
2018 Significantly altered peripheral blood cell DNA methylation profile as a result of immediate effect of metformin use in healthy individuals. Clinical epigenetics 29 30545422
2014 LIF upregulates poFUT1 expression and promotes trophoblast cell migration and invasion at the fetal-maternal interface. Cell death & disease 28 25165882
2015 O-Fucosylation of CCN1 is required for its secretion. FEBS letters 26 26424659
2019 ADAMTS9 and ADAMTS20 are differentially affected by loss of B3GLCT in mouse model of Peters plus syndrome. Human molecular genetics 25 31600785
2020 O-Fucosylation of ADAMTSL2 is required for secretion and is impacted by geleophysic dysplasia-causing mutations. The Journal of biological chemistry 24 32913123
2012 6-alkynyl fucose is a bioorthogonal analog for O-fucosylation of epidermal growth factor-like repeats and thrombospondin type-1 repeats by protein O-fucosyltransferases 1 and 2. Glycobiology 24 23045360
2018 O-Fucosylation of thrombospondin-like repeats is required for processing of microneme protein 2 and for efficient host cell invasion by Toxoplasma gondii tachyzoites. The Journal of biological chemistry 23 30538131
2016 Altered fucosyltransferase expression in the superior temporal gyrus of elderly patients with schizophrenia. Schizophrenia research 23 27773385
2006 Molecular evolution of protein O-fucosyltransferase genes and splice variants. Glycobiology 22 16679357
2018 Protein O-fucosyltransferase 2-mediated O-glycosylation of the adhesin MIC2 is dispensable for Toxoplasma gondii tachyzoite infection. The Journal of biological chemistry 17 30514763
2018 A perspective on structural and mechanistic aspects of protein O-fucosylation. Acta crystallographica. Section F, Structural biology communications 16 30084393
2025 FUT10 and FUT11 are protein O-fucosyltransferases that modify protein EMI domains. Nature chemical biology 15 39775168
2022 O-fucosylation of thrombospondin type 1 repeats is essential for ECM remodeling and signaling during bone development. Matrix biology : journal of the International Society for Matrix Biology 15 35167946
2018 Systematic Functional Characterization of Human 21st Chromosome Orthologs in Caenorhabditis elegans. G3 (Bethesda, Md.) 14 29367452
2004 The Caenorhabditis elegans ortholog of C21orf80, a potential new protein O-fucosyltransferase, is required for normal development. Genomics 14 15233996
2023 Fucosyltransferases Regulated by Fusobacterium Nucleatum and Act as Novel Biomarkers in Colon Adenocarcinoma. Journal of inflammation research 12 36852302
2019 Protein O-Fucosyltransferase 2 Is Not Essential for Plasmodium berghei Development. Frontiers in cellular and infection microbiology 12 31334132
2022 O-fucosylation stabilizes the TSR3 motif in thrombospondin-1 by interacting with nearby amino acids and protecting a disulfide bond. The Journal of biological chemistry 10 35597280
2025 Protein O-Fucosyltransferases: Biological Functions and Molecular Mechanisms in Mammals. Molecules (Basel, Switzerland) 8 40286076
2023 Emerging glyco-risk prediction model to forecast response to immune checkpoint inhibitors in colorectal cancer. Journal of cancer research and clinical oncology 7 36757621
2022 The Essential Role of Water Molecules in the Reaction Mechanism of Protein O-Fucosyltransferase 2. Angewandte Chemie (International ed. in English) 7 36260536
2024 Protein O-Fucosyltransferase Is Required for the Efficient Invasion of Hepatocytes by Plasmodium berghei Sporozoites. ACS infectious diseases 5 38421807
2025 Knockout of the fcsk gene in zebrafish causes neurodevelopmental defects. Zoological research 3 40049660
2020 Analyzing the Effects of O-Fucosylation on Secretion of ADAMTS Proteins Using Cell-Based Assays. Methods in molecular biology (Clifton, N.J.) 3 31463900
2017 Molecular cloning and functional expression of Lewis type α1,3/α1,4-fucosyltransferase cDNAs from Mangifera indica L. Phytochemistry 3 28910607
2025 IL-1β stimulates ADAMTS9 expression and contributes to preterm prelabor rupture of membranes. Cell communication and signaling : CCS 2 40057799
2023 O-fucosylation of thrombospondin type I repeats is dispensable for trafficking thrombospondin 1 to platelet secretory granules. Glycobiology 2 36721988
2023 Transcriptome research of human amniocytes identifies hub genes associated with developmental dysplasia in down syndrome. Aging 2 38095646
2026 Estradiol promotes trophoblasts syncytization by upregulating ESR2/SP1 transcription factor-mediated poFUT2 expression. Molecular and cellular endocrinology 1 41672297
2026 POFUT2 Mediated Fucosylation of JUP Enhances VEGFA Expression to Promote Angiogenesis in Colorectal Cancer. International journal of medical sciences 0 41583504
2026 REST deficiency and neurogenic-to-gliogenic shift in down syndrome human cerebral organoids. Molecular brain 0 42143345

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