Affinage

POFUT2

GDP-fucose protein O-fucosyltransferase 2 · UniProt Q9Y2G5

Length
429 aa
Mass
50.0 kDa
Annotated
2026-04-28
45 papers in source corpus 19 papers cited in narrative 19 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

POFUT2 is an ER-resident inverting O-fucosyltransferase that catalyzes the transfer of fucose from GDP-fucose to serine/threonine residues within the C-X-X-S/T-C consensus of folded thrombospondin type 1 repeats (TSRs), functioning as a non-canonical ER quality control checkpoint that promotes proper folding and efficient secretion of >40 TSR-containing extracellular matrix proteins including ADAMTS proteases, ADAMTSL proteins, CCN1, and ADAMTS13 (PMID:17395589, PMID:25544610, PMID:26424659). Crystal structures reveal a GT-B fold enzyme that recognizes the three-dimensional structure of folded TSRs rather than primary sequence, embracing nearly half the TSR surface through a dynamic network of water-mediated interactions and employing an SN2 inverting mechanism with water-assisted proton transfer (PMID:22588082, PMID:26854667, PMID:36260536). The O-fucose modification, often elongated to a Glc-β1,3-Fuc disaccharide by B3GLCT, stabilizes TSR disulfide bonds and domain folding additively, and loss of this modification impairs secretion of client proteins leading to disrupted ECM remodeling, aberrant BMP/TGF-β/Nodal signaling, and developmental defects including embryonic lethality, skeletal dysplasia, and geleophysic dysplasia (PMID:20637190, PMID:35167946, PMID:32913123, PMID:35597280). Pofut2-null mouse embryos phenocopy Adamts9 loss, establishing ADAMTS9 as a critical in vivo substrate, while disease mutations in ADAMTSL2 that abolish O-fucosylation sites provide a direct molecular mechanism for geleophysic dysplasia (PMID:27297885, PMID:32913123).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 2003 Low

    Establishing POFUT2 as a distinct fucosyltransferase family: phylogenetic analysis identified POFUT2 as a separate family sharing ancestral motifs with POFUT1 and other fucosyltransferases, but its enzymatic substrates and biological function were unknown.

    Evidence Phylogenetic and motif analysis across fucosyltransferase superfamily members

    PMID:12966037

    Open questions at the time
    • Computational analysis only, no experimental validation of enzymatic activity
    • No substrates identified
    • No biological phenotype assessed
  2. 2006 High

    Defining the sequential two-step glycosylation pathway: reconstitution showed POFUT2 must first add O-fucose to TSRs before B3GLCT can extend it with glucose, establishing the biosynthetic order and the Glc-β1,3-Fuc disaccharide product.

    Evidence In vitro sequential enzyme assay with recombinant POFUT2 and B3GLCT on bacterially expressed TSR, TLC and β-glucosidase characterization

    PMID:16899492

    Open questions at the time
    • Biological significance of glucose extension versus fucose alone not yet tested
    • In vivo stoichiometry of disaccharide unknown
  3. 2007 High

    Demonstrating that POFUT2-mediated O-fucosylation is required for secretion of TSR-containing proteins: loss of POFUT2 or GDP-fucose, or mutation of O-fucosylation sites, reduced secretion of ADAMTS13 and ADAMTSL1, establishing O-fucosylation as a secretion-promoting modification.

    Evidence Mass spectrometry, metabolic labeling, site-directed mutagenesis, siRNA knockdown, and expression in GDP-fucose-deficient Lec-13 cells for both ADAMTS13 and ADAMTSL1

    PMID:17395588 PMID:17395589

    Open questions at the time
    • Mechanism by which loss of fucosylation impairs secretion (folding vs. trafficking) not resolved
    • Number and identity of all POFUT2 substrates unknown
  4. 2010 High

    Establishing essential in vivo roles: Pofut2 knockout mouse embryos died with unrestricted EMT, defective mesoderm patterning, and expanded Nodal/BMP4 signaling, demonstrating that POFUT2-dependent O-fucosylation of ECM proteins is essential for embryonic development.

    Evidence Gene-trap mouse knockout (two alleles), immunofluorescence, in situ hybridization, teratoma assay

    PMID:20637190

    Open questions at the time
    • Which specific POFUT2 substrate(s) cause the embryonic phenotype not identified
    • Cell-autonomous vs. non-autonomous roles not distinguished
  5. 2012 High

    Revealing POFUT2 structural architecture and substrate recognition principle: crystal structures showed a GT-B fold and demonstrated that POFUT2 recognizes the conserved 3D fold of TSRs rather than primary sequence, explaining how a single enzyme can modify diverse TSR-containing proteins.

    Evidence X-ray crystallography of human POFUT2, steady-state kinetics with wild-type and mutant enzymes, mini-TSR substrate engineering

    PMID:22588082

    Open questions at the time
    • No enzyme-substrate co-crystal structure yet
    • Catalytic mechanism not resolved at atomic level
  6. 2014 High

    Defining a non-canonical ER quality control mechanism: O-fucosylation by POFUT2 occurs co-translationally on folded TSRs, stabilizes their disulfide bonds additively with B3GLCT-added glucose, and accelerates net TSR folding, establishing POFUT2 as an ER quality control enzyme rather than simply a secretion signal.

    Evidence Mass spectrometry of secreted vs. ER-retained protein intermediates, in vitro unfolding/refolding reconstitution with POFUT2 under redox conditions, siRNA and secretion assays

    PMID:25544610

    Open questions at the time
    • Whether POFUT2 interacts with canonical ER chaperones unknown
    • Whether the enzyme has lectin-like folding-sensor activity beyond its catalytic role not tested
  7. 2016 High

    Resolving the enzyme-substrate complex and catalytic mechanism: co-crystal structure of CePOFUT2-GDP-TSR1 showed POFUT2 embraces nearly half the TSR surface via water-mediated interactions and uses an inverting mechanism with a catalytic base, and genetic epistasis in mice demonstrated ADAMTS9 as the critical in vivo POFUT2 substrate for gastrulation.

    Evidence X-ray crystallography of CePOFUT2-GDP-TSR1 complex, MD simulations, mutagenesis; mouse conditional KO of Pofut2 and Adamts9, CRISPR KO secretion assays

    PMID:26854667 PMID:27297885

    Open questions at the time
    • Only group 1 TSR co-crystallized; group 2 TSR recognition untested structurally
    • Full transition-state characterization missing
  8. 2019 High

    Distinguishing the contributions of fucosylation versus glucose extension: B3glct knockout mice showed that glucose elongation of POFUT2-added fucose is differentially required for secretion of specific substrates (ADAMTS20 vs. ADAMTS9), with distinct developmental phenotypes, establishing that the disaccharide acts as a graded quality control signal.

    Evidence Mouse B3glct knockout (two alleles), genetic epistasis, secretion assays

    PMID:31600785

    Open questions at the time
    • Structural basis for why some TSRs require glucose extension for secretion and others do not is unknown
    • Quantitative relationship between glycan stoichiometry and secretion efficiency not defined
  9. 2020 High

    Connecting POFUT2 to human disease: ADAMTSL2 secretion requires POFUT2 but not B3GLCT, and a geleophysic dysplasia mutation (S641L) in TSR3 eliminates its O-fucosylation site, providing a direct molecular mechanism linking POFUT2-dependent fucosylation to the skeletal disease geleophysic dysplasia.

    Evidence Mass spectrometry of glycan modifications, POFUT2−/− and B3GLCT−/− cell secretion assays, disease mutation analysis

    PMID:32913123

    Open questions at the time
    • Whether other geleophysic dysplasia mutations act through the same O-fucosylation-dependent mechanism not tested
    • No patient-derived cells or rescue experiments
  10. 2022 High

    Elucidating the molecular mechanism of glycan-mediated TSR stabilization and extending POFUT2 roles to skeletal development: crystallographic/NMR evidence showed the Glc-Fuc disaccharide protects specific disulfide bonds via direct amino acid contacts, while conditional Pofut2 deletion in limb mesenchyme caused skeletal dysplasia with disrupted BMP/IHH and TGF-β signaling and aberrant ECM remodeling.

    Evidence X-ray crystallography, NMR, MD simulations, mutagenesis, in vitro unfolding assays; Prrx1-Cre conditional KO mice, signaling pathway analysis

    PMID:35167946 PMID:35597280 PMID:36260536

    Open questions at the time
    • Full QM/MM transition-state for human POFUT2 not computed
    • Which specific TSR-containing substrates mediate the skeletal phenotype not identified
    • Whether POFUT2 has non-catalytic functions remains untested
  11. 2025 Medium

    Identifying tissue-specific transcriptional regulation and new functional contexts: NF-κB/IL-1β drives POFUT2 expression in fetal membranes to enhance ADAMTS9-mediated versican degradation, while ESR2/SP1 drives POFUT2 in trophoblasts to promote syncytialization, expanding POFUT2 roles to parturition and placentation.

    Evidence ChIP and luciferase reporter assays, primary human amniotic epithelial cells, murine intra-amniotic IL-1β injection, NF-κB inhibitor rescue; ChIP for ESR2/SP1, trophoblast fusion assays, preeclampsia tissue IHC

    PMID:40057799 PMID:41672297

    Open questions at the time
    • Whether other POFUT2 substrates beyond ADAMTS9 contribute to fetal membrane weakening unknown
    • Causal role of reduced POFUT2 in preeclampsia not established beyond association
    • No genetic confirmation in human pregnancies

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the full repertoire of physiologically relevant POFUT2 substrates in vivo, whether POFUT2 has non-catalytic chaperone or sensor functions, the structural basis for substrate-selective dependence on glucose extension, and whether POFUT2 dysfunction directly causes Mendelian disease in humans.
  • No complete in vivo substrate catalog
  • No human genetic disease directly attributed to POFUT2 mutations
  • Non-catalytic functions not tested

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016740 transferase activity 9
Localization
GO:0005783 endoplasmic reticulum 2
Pathway
R-HSA-392499 Metabolism of proteins 5 R-HSA-9609507 Protein localization 5 R-HSA-1266738 Developmental Biology 3 R-HSA-1474244 Extracellular matrix organization 3
Partners
ADAMTS13ADAMTS9ADAMTSL1ADAMTSL2B3GLCTCCN1

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2007 POFUT2 adds O-linked fucose to thrombospondin type 1 repeats (TSRs) of ADAMTS13, and this O-fucosylation is required for efficient secretion of ADAMTS13; siRNA knockdown of POFUT2 or expression in GDP-fucose-deficient cells reduces ADAMTS13 secretion, and mutation of individual O-fucosylation sites reduces secretion. Mass spectrometry of tryptic peptides, metabolic labeling with [3H]fucose, site-directed mutagenesis of O-fucosylation sites, siRNA knockdown of POFUT2, expression in Lec-13 (GDP-fucose-deficient) cells The Journal of biological chemistry High 17395589
2007 POFUT2 O-fucosylates TSRs of ADAMTS-like-1/punctin-1 (at TSR2, TSR3, TSR4), and this modification is required for efficient secretion; mutation of O-fucosylation sites or expression in GDP-fucose-deficient Lec-13 cells reduces secreted punctin-1 levels. Mass spectrometry of tryptic peptides, metabolic labeling, site-directed mutagenesis, expression in Lec-13 cells with/without exogenous L-fucose The Journal of biological chemistry High 17395588
2006 A novel β1,3-glucosyltransferase (B3GLCT/β3Glc-T) elongates the O-fucose added by POFUT2 on TSR domains to form a Glcβ1-3Fuc disaccharide; POFUT2 must first fucosylate the TSR before it becomes an acceptor for B3GLCT, establishing the sequential order of modification in the ER. Recombinant enzyme expression, TLC analysis of reaction products, β-glucosidase digestion, in vitro sequential enzyme assay with recombinant POFUT2 and B3GLCT on bacterially expressed TSR domain Glycobiology High 16899492
2010 Mouse POFUT2 specifically adds O-fucose to TSRs and is essential for embryonic development; Pofut2 gene-trap mutant embryos exhibit unrestricted epithelial-to-mesenchymal transition, defective mesoderm patterning, loss of epiblast pluripotency, and expanded Nodal/BMP4/Fgf8/Wnt3 signaling, consistent with POFUT2 targets being ECM components. Gene-trap mouse knockout, immunofluorescence, in situ hybridization, teratoma formation assay Developmental biology High 20637190
2012 Crystal structures of human POFUT2 reveal a GT-B fold variation with distinct sugar-donor (GDP-fucose) and TSR-acceptor binding sites; kinetic and mutagenesis studies show that substrate specificity is determined by recognition of the conserved 3D fold of the TSR rather than its primary sequence. X-ray crystallography of POFUT2, steady-state kinetics of wild-type and mutant POFUT2 and TSR substrates, mini-TSR substrate engineering The EMBO journal High 22588082
2014 POFUT2 mediates a non-canonical ER quality control mechanism: it recognizes and glycosylates folded TSRs co-translationally, stabilizing them; mass spectral analysis shows TSRs in mature secreted protein are stoichiometrically modified whereas ER-resident folding intermediates are partially modified; in vitro unfolding and refolding assays show O-fucose and O-glucose stabilize TSRs additively and POFUT2 accelerates net TSR folding. Mass spectrometry of secreted vs. ER-retained protein, in vitro unfolding assays, in vitro refolding under redox conditions with recombinant POFUT2, siRNA knockdown, secretion assays Current biology : CB High 25544610
2016 Crystal structure of C. elegans POFUT2 in complex with GDP and human TSR1 reveals an inverting mechanism for fucose transfer assisted by a catalytic base; POFUT2 embraces nearly half the TSR1 surface using a small number of direct contacts and a large network of water-mediated interactions; mutagenesis shows POFUT2 prefers threonine over serine and requires the folded TSR consensus C-X-X-S/T-C. X-ray crystallography of CePOFUT2-GDP-TSR1 fusion complex, site-directed mutagenesis, atomic-level MD simulations Nature chemical biology High 26854667
2016 Loss of POFUT2 in mouse embryos phenocopies loss of ADAMTS9, and CRISPR/Cas9 knockout of POFUT2 in HEK293T cells blocks secretion of ADAMTS9; conditional deletion of Pofut2 or Adamts9 in epiblast rescues gastrulation defects, indicating that defects in POFUT2 mutant embryos are primarily caused by impaired O-fucosylation and secretion of ADAMTS9 from extraembryonic tissues. Mouse knockouts (Pofut2 and Adamts9), Cre-mediated conditional deletion, CRISPR/Cas9 knockout in HEK293T cells, secretion assays, genetic epistasis Developmental biology High 27297885
2015 CCN1 (Cyr61) is O-fucosylated at Thr242 within its TSR1 domain by POFUT2; knockdown of POFUT2 reduces secreted and cell-surface levels of CCN1, demonstrating that O-fucosylation at this site regulates CCN1 secretion. Mass spectrometry identification of O-fucosylation site, site-directed mutagenesis (T242A), POFUT2 siRNA knockdown, secretion and cell-surface localization assays FEBS letters High 26424659
2017 O-glycosylation of EGF repeats by POGLUT1 and POFUT1 (not POFUT2) cooperatively stabilizes individual EGF repeat domains through intramolecular interactions; crystal structure of an EGF repeat with O-glucose trisaccharide at 2.2 Å shows the glycan fills a surface groove with multiple protein contacts; this mechanism is analogous to POFUT2's role on TSRs. Crystal structure of glycosylated EGF repeat, in vitro EGF repeat unfolding assays, cell-surface Notch1 expression assays in HEK293T POGLUT1/POFUT1 knockout cells The Journal of biological chemistry Medium 28729422
2020 ADAMTSL2 TSRs are modified with glucose-fucose disaccharide at high stoichiometry by POFUT2/B3GLCT; ADAMTSL2 secretion is lost in POFUT2−/− but not B3GLCT−/− cells; two GPHYSD1 disease mutations (S641L in TSR3, G817R in TSR6) reduce ADAMTSL2 secretion, and S641L eliminates O-fucosylation of TSR3, providing a molecular mechanism for geleophysic dysplasia. Mass spectrometry of glycan modifications, POFUT2−/− and B3GLCT−/− cell secretion assays, disease mutant analysis by MS and secretion assay The Journal of biological chemistry High 32913123
2022 The Glc-Fuc disaccharide on TSR3 of thrombospondin-1 interacts with specific nearby amino acids to protect a disulfide bond; crystallographic, NMR, and MD evidence show these interactions stabilize the folded TSR; mutation of the interacting amino acids reduces the stabilizing effect of the sugars in vitro, providing a molecular mechanism for POFUT2-mediated ER quality control. X-ray crystallography, NMR spectroscopy, molecular dynamics simulations, site-directed mutagenesis, in vitro unfolding assays The Journal of biological chemistry High 35597280
2022 Conditional knockout of Pofut2 in limb mesenchyme causes limb shortening and skeletal dysplasia with accumulation of fibrillin 2, decreased BMP/IHH signaling, and increased TGF-β signaling, demonstrating that O-fucosylation of TSR-containing ECM proteins by POFUT2 is required for normal ECM remodeling and signaling during bone development. Cre-mediated conditional knockout (Prrx1-Cre), immunofluorescence, signaling pathway analysis, in vitro secretion assays in POFUT2-null HEK293T cells Matrix biology : journal of the International Society for Matrix Biology High 35167946
2022 POFUT2 follows a classical SN2 inverting glycosyltransferase 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; crystal structure of CePOFUT2 with a TSR from group 2 confirms similar recognition of TSRs from both group 1 and 2. X-ray crystallography of CePOFUT2-TSR group 2 complex, QM/MM computational analysis of reaction mechanism using human POFUT2 as model Angewandte Chemie (International ed. in English) High 36260536
2025 POFUT2 interacts with and fucosylates Junction Plakoglobin (JUP) in colorectal cancer cells; this fucosylation upregulates JUP protein levels and subsequently increases VEGFA expression to promote angiogenesis. Flag-immunoprecipitation with mass spectrometry, co-immunoprecipitation, western blot, angiogenesis assays with conditioned medium, immunohistochemistry International journal of medical sciences Medium 41583504
2026 Estradiol upregulates POFUT2 expression in trophoblasts via the ESR2/SP1 transcription factor complex binding to the POFUT2 promoter; elevated POFUT2 promotes trophoblast syncytialization (cell fusion), and POFUT2 expression is decreased in syncytiotrophoblast of preeclampsia placentas. Chromatin immunoprecipitation (ChIP), co-immunoprecipitation of ESR2/SP1, siRNA knockdown of POFUT2, trophoblast fusion cell model, immunohistochemistry Molecular and cellular endocrinology Medium 41672297
2025 NF-κB activated by IL-1β binds to the POFUT2 promoter and upregulates POFUT2 expression; elevated POFUT2 then enhances ADAMTS9 secretion (via O-fucosylation), promoting versican degradation and ECM weakening in fetal membranes. ChIP and luciferase reporter assays for NF-κB binding to POFUT2 promoter, primary human amniotic epithelial cell IL-1β treatment, murine intra-amniotic IL-1β injection model, NF-κB inhibitor rescue Cell communication and signaling : CCS Medium 40057799
2003 POFUT2 constitutes a distinct protein O-fucosyltransferase family (family 2) that shares three conserved peptide motifs with POFUT1, α2-fucosyltransferases, and α6-fucosyltransferases, defining a new superfamily of fucosyltransferases with a common ancestral origin. Phylogenetic analysis, sequence motif identification, comparative genomics Glycobiology Low 12966037
2019 B3GLCT loss differentially affects secretion of ADAMTS9 and ADAMTS20 compared to POFUT2 loss, with hydrocephalus and white spotting in B3glct mutant mice resulting from loss of ADAMTS20, eye defects from partial reduction of ADAMTS9, and cleft palate from combined loss; this demonstrates that B3GLCT-mediated glucose extension of POFUT2-added fucose is required for a subset of POFUT2 targets. Mouse B3glct knockout (two alleles), genetic epistasis, biochemical secretion assays Human molecular genetics High 31600785

Source papers

Stage 0 corpus · 45 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 220 10942434
2017 O-Glycosylation modulates the stability of epidermal growth factor-like repeats and thereby regulates Notch trafficking. The Journal of biological chemistry 92 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 83 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 55 26854667
2003 A new superfamily of protein-O-fucosyltransferases, alpha2-fucosyltransferases, and alpha6-fucosyltransferases: phylogeny and identification of conserved peptide motifs. Glycobiology 55 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 32 30101373
2018 Significantly altered peripheral blood cell DNA methylation profile as a result of immediate effect of metformin use in healthy individuals. Clinical epigenetics 28 30545422
2014 LIF upregulates poFUT1 expression and promotes trophoblast cell migration and invasion at the fetal-maternal interface. Cell death & disease 27 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
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
2020 O-Fucosylation of ADAMTSL2 is required for secretion and is impacted by geleophysic dysplasia-causing mutations. The Journal of biological chemistry 22 32913123
2006 Molecular evolution of protein O-fucosyltransferase genes and splice variants. Glycobiology 22 16679357
2018 A perspective on structural and mechanistic aspects of protein O-fucosylation. Acta crystallographica. Section F, Structural biology communications 16 30084393
2018 Protein O-fucosyltransferase 2-mediated O-glycosylation of the adhesin MIC2 is dispensable for Toxoplasma gondii tachyzoite infection. The Journal of biological chemistry 16 30514763
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 14 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 9 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
2023 O-fucosylation of thrombospondin type I repeats is dispensable for trafficking thrombospondin 1 to platelet secretory granules. Glycobiology 2 36721988
2025 IL-1β stimulates ADAMTS9 expression and contributes to preterm prelabor rupture of membranes. Cell communication and signaling : CCS 1 40057799
2023 Transcriptome research of human amniocytes identifies hub genes associated with developmental dysplasia in down syndrome. Aging 1 38095646
2026 POFUT2 Mediated Fucosylation of JUP Enhances VEGFA Expression to Promote Angiogenesis in Colorectal Cancer. International journal of medical sciences 0 41583504
2026 Estradiol promotes trophoblasts syncytization by upregulating ESR2/SP1 transcription factor-mediated poFUT2 expression. Molecular and cellular endocrinology 0 41672297