Affinage

OGT

UDP-N-acetylglucosamine--peptide N-acetylglucosaminyltransferase 110 kDa subunit · UniProt O15294

Length
1046 aa
Mass
116.9 kDa
Annotated
2026-06-10
100 papers in source corpus 27 papers cited in narrative 27 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

OGT is an essential glycosyltransferase that installs O-GlcNAc on serine/threonine residues of nuclear and cytoplasmic substrates to control protein stability, localization, and signaling across diverse cellular processes (PMID:33419956, PMID:35230102). Cryo-EM and crystallographic studies define OGT as a scissor-shaped dimer whose extended substrate-binding groove accommodates peptide substrates, and within the OGT–OGA complex a flexible OGA segment occupies this groove while OGT occludes the OGA active site, establishing reciprocal inhibition that maintains O-GlcNAc homeostasis (PMID:37907462, PMID:29723473). Beyond glycosylation, OGT's glycosyltransferase activity is required for mammalian cell proliferation while its HCF-1 protease activity is dispensable, and a noncatalytic scaffolding function — impacting oxidative phosphorylation and actin cytoskeleton proteins — is itself sufficient to sustain cell growth (PMID:33419956, PMID:26305326). A recurring mechanistic theme is that OGT-catalyzed O-GlcNAcylation alters substrate fate: it stabilizes c-Myc (Ser415), SMAD4 (Thr63, by blocking GSK-3β-mediated degradation), and KAT5/TIP60 to drive cancer metabolism, TGF-β signaling, and metastasis, destabilizes RIPK3 to restrain necroptosis, and tunes enzyme activity such as eNOS dimerization and SLC7A11-mediated cystine import (PMID:38778217, PMID:33199824, PMID:34650217, PMID:31672932, PMID:32863226, PMID:37867237); globally, O-GlcNAc bidirectionally regulates protein thermostability, more often destabilizing than stabilizing its targets (PMID:35230102). OGT also suppresses mTOR hyperactivation by restraining proteasome activity, and dampens macrophage proinflammatory signaling by O-GlcNAcylating S6K1 to block its phosphorylation (PMID:36626549, PMID:32601203). Tissue-specific OGT loss produces distinct phenotypes — demyelinating neuropathy through mislocalized Periaxin, sensory neuron dieback, synaptic AMPA receptor and dendritic spine defects, astrocytic regulation of glutamate transport, and impaired pancreatic α- and β-cell function — reflecting substrate-specific roles in neural and metabolic tissues (PMID:27629714, PMID:28115479, PMID:28143929, PMID:36757814, PMID:33460647, PMID:34462257).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 2013 Medium

    Established a chromatin-targeting mechanism for OGT by showing it is recruited and stabilized through a direct protein partner, addressing how a promiscuous enzyme gains spatial specificity.

    Evidence Affinity purification/MS, Co-IP with TET3 deletion mutants, and chromatin fractionation

    PMID:24304661

    Open questions at the time
    • TET3 O-GlcNAcylation had no effect on TET3 5mC hydroxylation, leaving the functional consequence of the modification unclear
    • whether other partners recruit OGT to chromatin not addressed
  2. 2014 High

    Showed OGT regulates autophagy through SNARE glycosylation, linking nutrient-sensing O-GlcNAc to membrane fusion.

    Evidence OGT knockdown, SNAP-29 O-GlcNAc site mutagenesis, and autophagic flux assays in mammalian cells and C. elegans

    PMID:25419848

    Open questions at the time
    • does not resolve how nutrient state quantitatively controls SNAP-29 modification stoichiometry
    • structural basis of glycosylation impairing SNARE assembly not defined
  3. 2015 Medium

    Defined the sequence determinants in HCF-1 that govern OGT's proteolytic versus glycosyltransferase outcomes within the same active site.

    Evidence Mutagenesis of HCF-1PRO cleavage sites with OGT binding and protease activity assays

    PMID:26305326

    Open questions at the time
    • does not establish the physiological consequence of HCF-1 cleavage
    • single-lab biochemical characterization
  4. 2016 Medium

    Identified a substrate-specific role for OGT in myelin maintenance by linking Periaxin O-GlcNAcylation to its correct localization.

    Evidence Schwann cell-specific OGT knockout, MS proteomics of sciatic nerve, PRX immunofluorescence, and electrophysiology

    PMID:27629714

    Open questions at the time
    • does not prove PRX glycosylation alone accounts for the full neuropathy
    • site of PRX O-GlcNAcylation and its direct effect on localization not mapped
  5. 2017 Medium

    Localized OGT to the postsynaptic density and demonstrated it is required for excitatory synapse composition and dendritic spine maturation, and separately that sensory neurons depend on OGT for survival.

    Evidence PSD fractionation, neuron- and sensory-neuron-specific OGT knockout, AMPA subunit immunostaining, spine and innervation quantification

    PMID:28115479 PMID:28143929

    Open questions at the time
    • specific synaptic substrates of OGT not identified
    • molecular cause of axonal dieback preceding cell death not defined
  6. 2018 Medium

    Extended OGT's role to substrate stabilization in cancer and to substrate-recognition specificity, showing it glycosylates c-Myc (S415) to drive tumor metabolism and selectively recognizes a lamin A 'sweet spot.'

    Evidence Site-directed mutagenesis, ChIP, metabolic flux, xenografts; in vitro glycosylation of recombinant lamin tails with MS site mapping

    PMID:29772801 PMID:38778217

    Open questions at the time
    • determinants of OGT substrate selectivity remain largely empirical
    • lamin A glycosylation's nuclear function not established
  7. 2019 Medium

    Linked OGT to control of programmed necrosis by showing RIPK3 O-GlcNAcylation reduces its stability and restrains hepatocyte necroptosis.

    Evidence Liver-specific OGT knockout mice, RIPK3/MLKL immunoblotting, O-GlcNAcylation assays, histology

    PMID:31672932

    Open questions at the time
    • RIPK3 O-GlcNAc site not defined
    • mechanism connecting glycosylation to degradation not resolved
  8. 2020 Medium

    Demonstrated OGT acts as a brake on inflammatory and signaling pathways via substrate modifications affecting phosphorylation, glycosylation of S6K1 suppressing mTORC1 and of eNOS controlling its dimerization and activity.

    Evidence Macrophage and tissue OGT knockouts, S6K1 and eNOS O-GlcNAc/phospho assays, dimerization and activity assays, mouse models

    PMID:32601203 PMID:32863226

    Open questions at the time
    • crosstalk between O-GlcNAc and phosphorylation sites mechanistically incomplete
    • SIRT1-CREB control of OGT expression (Low confidence) not independently confirmed
  9. 2021 High

    Resolved the essentiality logic of OGT by separating its glycosyltransferase, protease, and noncatalytic functions, and broadened its substrate network across DNA repair, metastasis, and pancreatic endocrine function.

    Evidence Separation-of-function complementation with degron depletion and proteomics; plus mutagenesis/Co-IP/ChIP studies on PARG, KAT5, MTA1, and conditional α/β-cell knockouts

    PMID:33419956 PMID:33460647 PMID:34019948 PMID:34462257 PMID:34650217 PMID:37858678

    Open questions at the time
    • molecular identity of the noncatalytic scaffolding activity not defined
    • how OGT coordinates so many substrates within one tissue unresolved
  10. 2022 Medium

    Provided a proteome-wide view showing O-GlcNAc bidirectionally tunes protein thermostability, reframing the modification as a broad regulator of complex assembly rather than uniformly stabilizing.

    Evidence Thermal proteome profiling comparing OGA-inhibitor-treated and control cells with orthogonal validation

    PMID:35230102

    Open questions at the time
    • whether stability changes are direct or secondary not always resolved
    • OGA inhibition reflects global O-GlcNAc, not OGT activity per se
  11. 2023 High

    Defined the structural basis of O-GlcNAc homeostasis through mutual OGT–OGA inhibition and placed OGT mechanistically upstream of mTOR via proteasome suppression.

    Evidence Cryo-EM of OGT alone and OGT–OGA complex; genome-wide CRISPR screen, phospho-proteomics, and mTOR/mitochondrial assays; USP8 deubiquitination of OGT

    PMID:36626549 PMID:37867237 PMID:37907462

    Open questions at the time
    • how the OGT–OGA setpoint is tuned in cells not established
    • link between proteasome suppression and the noncatalytic essential function unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • The molecular basis of OGT's essential noncatalytic scaffolding function and the general rules governing its selection among thousands of substrates remain unresolved.
  • no defined structural/biochemical mechanism for the noncatalytic essential role
  • no predictive substrate-recognition code beyond the dimer groove
  • tissue-specific substrate prioritization not explained

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016740 transferase activity 5 GO:0140096 catalytic activity, acting on a protein 2 GO:0016787 hydrolase activity 1
Localization
GO:0005634 nucleus 2 GO:0005829 cytosol 2 GO:0005886 plasma membrane 1
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-392499 Metabolism of proteins 3 R-HSA-5357801 Programmed Cell Death 1 R-HSA-73894 DNA Repair 1 R-HSA-9612973 Autophagy 1
Partners
GSK-3BHCF-1OGAPCNATET3USP8

Evidence

Reading pass · 27 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2014 OGT mediates O-GlcNAcylation of the SNARE protein SNAP-29; OGT knockdown or mutation of O-GlcNAc sites in SNAP-29 promotes formation of a SNAP-29-containing SNARE complex, increases autophagosome-endosome/lysosome fusion, and promotes autophagic flux in mammalian cells and C. elegans. OGT knockdown, site-directed mutagenesis of O-GlcNAc sites in SNAP-29, autophagic flux assays, genetic depletion of ogt-1 in C. elegans Nature cell biology High 25419848
2023 Cryo-EM structures reveal that human OGT forms a functionally important scissor-shaped dimer, and within the OGT-OGA complex, a long flexible OGA segment occupies OGT's extended substrate-binding groove and positions a serine for O-GlcNAcylation, while OGT simultaneously disrupts the functional dimerization of OGA and occludes its active site—establishing mutual inhibition between OGT and OGA as a mechanism maintaining O-GlcNAc homeostasis. Cryo-electron microscopy structure determination of human OGT alone and in complex with OGA Nature communications High 37907462
2021 OGT's glycosyltransferase activity is required for mammalian cell proliferation, but its protease activity (HCF-1 cleavage) is dispensable for viability; additionally, OGT has an essential noncatalytic role sufficient to rescue cell growth when catalytically inactive OGT is added back to OGT-depleted cells. Noncatalytic OGT functions especially impact proteins involved in oxidative phosphorylation and the actin cytoskeleton. Genetic complementation with separation-of-function OGT variants; auxin-inducible degron to deplete endogenous OGT; quantitative proteomics Proceedings of the National Academy of Sciences of the United States of America High 33419956
2023 USP8 stabilizes OGT protein by inhibiting K48-specific poly-ubiquitination of OGT at the K117 site; STE20-like kinase (SLK)-mediated S716 phosphorylation of USP8 is required for its interaction with OGT. OGT in turn O-GlcNAcylates SLC7A11 at Ser26, which is required for SLC7A11-mediated cystine import. Co-immunoprecipitation, ubiquitination assays, mutagenesis (K117, S716), OGT depletion/overexpression, in vivo xenograft and metastasis models, intracellular cystine/GSH measurements Advanced science (Weinheim, Baden-Wurttemberg, Germany) Medium 37867237
2019 OGT O-GlcNAcylates RIPK3, which is associated with reduced RIPK3 protein stability; liver-specific OGT knockout leads to elevated RIPK3 and MLKL expression, excessive hepatocyte necroptosis, and progression to liver fibrosis. Liver-specific OGT knockout mice, immunoblotting for RIPK3 and MLKL, O-GlcNAcylation assays, histology JCI insight Medium 31672932
2020 OGT inhibits macrophage proinflammatory activation by catalyzing O-GlcNAcylation of S6K1 (ribosomal protein S6 kinase beta-1), which suppresses S6K1 phosphorylation and downstream mTORC1 signaling. OGT knockout in macrophages, S6K1 O-GlcNAcylation assays, phosphorylation assays, high-fat diet mouse model, adipose tissue inflammation and insulin resistance measurements Proceedings of the National Academy of Sciences of the United States of America Medium 32601203
2023 OGT controls mammalian cell viability through suppression of proteasome activity; in the absence of OGT, increased proteasome activity raises steady-state amino acid levels, driving mTOR lysosomal translocation and hyperactivation, increased oxidative phosphorylation, and ultimately mitochondrial dysfunction that blocks cell proliferation. Genome-wide CRISPR-Cas9 screen in mouse embryonic stem cells, phospho-proteomics, mTOR activity assays, mitochondrial function assays, validation in CD8+ T cells Proceedings of the National Academy of Sciences of the United States of America High 36626549
2017 OGT is enriched in the postsynaptic density of excitatory synapses; OGT knockout in postsynaptic neurons decreases synaptic expression of GluA2 and GluA3 AMPA receptor subunits (but not GluA1), reduces the number of opposed excitatory presynaptic terminals, and results in fewer and less mature dendritic spines. Postsynaptic density fractionation, neuron-specific OGT knockout, immunostaining of AMPA receptor subunits, spine morphology analysis Proceedings of the National Academy of Sciences of the United States of America Medium 28143929
2023 In astrocytes of the medial prefrontal cortex, OGT modulates glutamatergic synaptic transmission through O-GlcNAcylation of glutamate transporter-1 (GLT-1); astrocyte-specific OGT knockout produces antidepressant-like effects and preserves neuronal morphology and Ca2+ activity deficits caused by chronic stress. Astrocyte-specific OGT knockout mice, chronic social-defeat stress model, Ca2+ imaging, O-GlcNAcylation assays for GLT-1, behavioral assays The Journal of clinical investigation Medium 36757814
2016 SC-specific OGT deletion causes tomaculous demyelinating neuropathy with progressive demyelination and axonal loss; Periaxin (PRX) is an O-GlcNAcylated myelin protein that is mislocalized within the myelin sheath when O-GlcNAcylation is absent, and phenotypes of OGT-SCKO mice closely resemble those of PRX-deficient mice. Schwann cell-specific OGT knockout mice, mass spectrometry-based proteomic identification of O-GlcNAcylated proteins in sciatic nerve, PRX localization by immunofluorescence, electrophysiology The Journal of neuroscience : the official journal of the Society for Neuroscience Medium 27629714
2017 Sensory neuron-specific OGT knockout in mice results in progressive loss of epidermal nerve fiber endings and dorsal root ganglion cell body loss, beginning postnatally; nerve-ending loss precedes cell body loss, indicating axonal dieback progressing to neuronal death. Adult-inducible OGT knockout produces a similar neuropathy. Sensory neuron-specific and inducible OGT knockout mice, epidermal innervation quantification, behavioral hyposensitivity assays, axon outgrowth assays in cultured neurons The Journal of neuroscience : the official journal of the Society for Neuroscience Medium 28115479
2013 TET3 physically interacts with OGT via its C-terminal H domain; TET3 is O-GlcNAcylated by OGT (though this does not affect global 5mC hydroxylation by TET3); TET3 interaction enhances OGT localization to chromatin by stabilizing OGT protein. Affinity purification/mass spectrometry of FLAG-TET3, Co-IP with deletion mutants, chromatin fractionation, O-GlcNAcylation assays Genes to cells : devoted to molecular & cellular mechanisms Medium 24304661
2015 OGT cleavage of HCF-1 at HCF-1PRO repeats is promoted by distinct OGT-binding sites: the glutamate at the cleavage site specifically inhibits OGT association (and UDP-GlcNAc cofactor binding), and a novel OGT-binding sequence near the first HCF-1PRO repeat enhances cleavage efficiency. Mutagenesis of HCF-1PRO repeat cleavage sites, OGT binding assays, protease activity assays, identification of novel OGT-binding sequence PloS one Medium 26305326
2018 OGT O-GlcNAcylates c-Myc at serine 415, increasing c-Myc stability; stabilized c-Myc transcriptionally upregulates PDK2 expression, which phosphorylates pyruvate dehydrogenase to inhibit mitochondrial pyruvate metabolism, suppress ROS, and promote colorectal tumor growth. OGT depletion/overexpression in colorectal cancer cells, site-directed mutagenesis of c-Myc S415, ChIP assay, metabolic flux measurements, xenograft tumor growth assay, clinical tissue correlation Cell death and differentiation Medium 38778217
2020 OGT O-GlcNAcylates eNOS at Ser-615, resulting in reduced eNOS dimerization and reduced eNOS activity; this Ser-615 modification controls Ser-1177 phosphorylation, establishing a regulatory mechanism of eNOS function under glucose dysregulation. Mass spectrometry identification of O-GlcNAc site on eNOS, mutagenesis of Ser-615, eNOS dimerization assays, activity assays, patient-derived IPAH samples Redox biology Medium 32863226
2020 O-GlcNAcylation of SMAD4 at Thr63 (catalyzed by OGT) inhibits interaction between SMAD4 and GSK-3β, thereby preventing GSK-3β-mediated proteasomal degradation and prolonging SMAD4 half-life; loss of this O-GlcNAcylation attenuates TGF-β/SMAD transcriptional reporter activity. Site-directed mutagenesis of SMAD4 Thr63, co-immunoprecipitation with GSK-3β, protein half-life assays, luciferase SMAD-binding-element reporter assay Scientific reports Medium 33199824
2018 A crystal structure of human OGT with a thio-linked UDP-peptide bisubstrate inhibitor reveals how the inhibitor mimics the pseudo-Michaelis complex; modular S-linked UDP-peptide conjugates inhibit OGT activity in HeLa cell lysates (Ki = 1.3 μM for the best compound). Crystal structure determination of hOGT-inhibitor complex; in vitro OGT inhibition assays with Ki measurement; fluorescence polarimetry assay Bioconjugate chemistry High 29723473
2021 OGT regulates β-cell mitochondrial morphology and bioenergetics through the transcription factor Pdx1; constitutive (but not inducible) β-cell OGT deletion causes swollen mitochondria, reduced glucose-stimulated oxygen consumption, and reduced ATP production; Pdx1 overexpression rescues mitochondrial dysfunction in βOGTKO islets. β-cell-specific constitutive and inducible OGT knockout mice, mitochondrial morphology imaging, Seahorse metabolic flux analysis, islet proteomics, Pdx1 overexpression rescue Diabetes Medium 34462257
2021 O-GlcNAcylation of PARG (ADP-ribose glycohydrolase) at Ser26 by OGT promotes PARG nuclear localization and chromatin association; upon DNA damage, O-GlcNAcylated PARG is recruited to damage sites and interacts with PCNA, enhancing poly(ADP-ribosyl)ation of DDB1, attenuating DDB1 auto-ubiquitination, and thereby stabilizing DDB1. O-GlcNAcylation site mapping by MS, mutagenesis of Ser26, subcellular fractionation, Co-IP with PCNA, PAR assays, ubiquitination assays, xenograft mouse models The Journal of biological chemistry Medium 37858678
2021 OGT O-GlcNAcylates KAT5 (TIP60), increasing KAT5 stability by suppressing its ubiquitination; O-GlcNAcylated KAT5 epigenetically activates TWIST1 expression via histone H4 acetylation and enhances MMP9/MMP14 expression via c-Myc acetylation, promoting EMT and HCC metastasis. PCK1 knockout hepatoma cells, KAT5 ubiquitination and stability assays, ChIP for histone H4 acetylation at TWIST1 promoter, c-Myc acetylation assays, loss-of-function and gain-of-function in vivo metastasis models Oncogene Medium 34650217
2018 OGT interacts with progesterone receptor (PR) and catalyzes O-GlcNAcylation of PR; O-GlcNAcylated PR is more transcriptionally active on PR-target genes despite decreased PR mRNA and total protein levels when O-GlcNAc levels are globally high. Co-immunoprecipitation of PR and OGT, O-GlcNAcylation assays of PR, transcriptional reporter assays on PR-target genes, OGT inhibitor and overexpression studies Hormones & cancer Low 28929346
2021 α-cell-specific OGT knockout mice (constitutive and inducible) show significantly reduced glucagon levels, lower α-cell glucagon content, impaired pyruvate-stimulated gluconeogenesis, and reduced in vitro glucagon secretion, demonstrating that OGT is required for α-cell function and glucagon secretion. Constitutive and inducible α-cell-specific OGT knockout mice, immunoblotting, immunofluorescence, metabolic phenotyping, in vitro glucagon secretion assays The Journal of biological chemistry Medium 33460647
2020 SIRT1 deacetylates CREB and inhibits its phosphorylation at Ser133; inactivated CREB suppresses OGT expression, thereby decreasing O-GlcNAcylation of tau and increasing tau phosphorylation at specific sites. SIRT1 overexpression/knockdown, CREB phosphorylation assays, OGT promoter activity, tau O-GlcNAcylation and phosphorylation measurements Aging Low 32310828
2018 OGT selectively O-GlcNAcylates lamin A (but not lamin C, lamin B1, or progerin/Δ50) at 11 sites in a 'sweet spot' unique to lamin A; residues deleted in Hutchinson-Gilford progeria (progerin Δ50) are required for substrate recognition/modification by OGT in vitro, and deletion Δ35 removes potential OGT-association motifs (residues 622–625 and 639–645). In vitro OGT glycosylation assay with purified recombinant lamin tails, mass spectrometry site mapping, deletion mutagenesis, detection in Huh7 cells and mouse liver Cells Medium 29772801
2021 OGT1-catalyzed O-GlcNAcylation of AKT1 enhances AKT1 protein stability and promotes its binding with FOXO1; O-GlcNAcylated AKT1 promotes FOXO1 phosphorylation at Ser238, preventing FOXO1 nuclear entry and reducing gabarapl1 promoter activity, thereby inhibiting glycophagy. OGT1 knockdown, AKT1 stability assays, Co-IP of AKT1 and FOXO1, dual-luciferase reporter assay, ChIP at gabarapl1 promoter, 13C-labeled LC-MS metabolite analysis, high-carbohydrate diet fish model The Journal of nutritional biochemistry Low 36990368
2022 Thermal proteome profiling reveals that O-GlcNAc bidirectionally regulates protein thermostability: 72 proteins display O-GlcNAc-dependent changes in stability, with the majority of O-GlcNAc-influenced proteins being destabilized rather than stabilized by the modification; destabilized proteins cluster into distinct macromolecular complexes. Thermal proteome profiling (TPP) comparing OGA inhibitor-treated vs. control cells, orthogonal validation of specific proteins Journal of the American Chemical Society Medium 35230102
2021 OGT O-GlcNAcylation of MTA1 at Ser237/241/246 in adriamycin-adaptive breast cancer cells promotes MTA1 interaction with chromatin and its association with the NuRD complex, altering genome-wide binding to gene promoters and transcriptional regulation of genotoxic stress adaptation genes. Quantitative proteomics, ChIP-seq, transcriptome analysis, mutagenesis of MTA1 O-GlcNAc sites, Co-IP with NuRD complex components Biochimica et biophysica acta. General subjects Medium 34019948

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2015 A little sugar goes a long way: the cell biology of O-GlcNAc. The Journal of cell biology 472 25825515
2005 The hexosamine signaling pathway: deciphering the "O-GlcNAc code". Science's STKE : signal transduction knowledge environment 406 16317114
2011 O-GlcNAc signalling: implications for cancer cell biology. Nature reviews. Cancer 387 21850036
2006 Cell signaling, the essential role of O-GlcNAc! Biochimica et biophysica acta 322 16781888
2010 O-GlcNAc signaling: a metabolic link between diabetes and cancer? Trends in biochemical sciences 293 20466550
2009 The hexosamine signaling pathway: O-GlcNAc cycling in feast or famine. Biochimica et biophysica acta 276 19647043
2013 O-GlcNAc cycling: a link between metabolism and chronic disease. Annual review of nutrition 263 23642195
2014 O-GlcNAc-modification of SNAP-29 regulates autophagosome maturation. Nature cell biology 245 25419848
2014 The emerging link between O-GlcNAc and Alzheimer disease. The Journal of biological chemistry 212 25336656
2010 Modulation of transcription factor function by O-GlcNAc modification. Biochimica et biophysica acta 202 20202486
2013 Cracking the O-GlcNAc code in metabolism. Trends in endocrinology and metabolism: TEM 198 23647930
2007 O-GlcNAc modification in diabetes and Alzheimer's disease. Molecular bioSystems 191 17940659
2014 Cancer metabolism and elevated O-GlcNAc in oncogenic signaling. The Journal of biological chemistry 178 25336642
2003 O-GlcNAc: a regulatory post-translational modification. Biochemical and biophysical research communications 159 12615051
2016 The Biochemistry of O-GlcNAc Transferase: Which Functions Make It Essential in Mammalian Cells? Annual review of biochemistry 151 27294441
2010 O-GlcNAc modification, insulin signaling and diabetic complications. Diabetes & metabolism 130 21074472
2010 O-GlcNAc signaling in the cardiovascular system. Circulation research 128 20651294
2013 O-GlcNAc in cancer biology. Amino acids 126 23836420
2012 O-GlcNAc processing enzymes: catalytic mechanisms, substrate specificity, and enzyme regulation. Current opinion in chemical biology 125 23146438
2016 Roles of O-GlcNAc in chronic diseases of aging. Molecular aspects of medicine 124 27259471
2009 O-GlcNAc protein modification in plants: Evolution and function. Biochimica et biophysica acta 122 19961900
2018 O-GlcNAc in cancer: An Oncometabolism-fueled vicious cycle. Journal of bioenergetics and biomembranes 116 29594839
2003 Dynamic interplay between O-GlcNAc and O-phosphate: the sweet side of protein regulation. Current opinion in structural biology 115 14568619
2014 O-GlcNAc signaling in cancer metabolism and epigenetics. Cancer letters 114 24769077
2013 O-GlcNAc and the cardiovascular system. Pharmacology & therapeutics 114 24287310
2018 O-GlcNAc as an Integrator of Signaling Pathways. Frontiers in endocrinology 112 30464755
2008 O-GlcNAc modification of transcription factors, glucose sensing and glucotoxicity. Trends in endocrinology and metabolism: TEM 105 18929495
2023 Targeting USP8 Inhibits O-GlcNAcylation of SLC7A11 to Promote Ferroptosis of Hepatocellular Carcinoma via Stabilization of OGT. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 101 37867237
2010 O-GlcNAc cycling: emerging roles in development and epigenetics. Seminars in cell & developmental biology 95 20488252
2021 O-GlcNAcylation and O-GlcNAc Cycling Regulate Gene Transcription: Emerging Roles in Cancer. Cancers 89 33916244
2017 O-GlcNAc transferase regulates excitatory synapse maturity. Proceedings of the National Academy of Sciences of the United States of America 78 28143929
2013 TET3-OGT interaction increases the stability and the presence of OGT in chromatin. Genes to cells : devoted to molecular & cellular mechanisms 75 24304661
2023 O-GlcNAc transferase in astrocytes modulates depression-related stress susceptibility through glutamatergic synaptic transmission. The Journal of clinical investigation 74 36757814
2014 O-GlcNAc transferase and O-GlcNAcase: achieving target substrate specificity. Amino acids 73 25173736
2022 Demystifying the O-GlcNAc Code: A Systems View. Chemical reviews 71 35302357
2019 O-GlcNAc transferase suppresses necroptosis and liver fibrosis. JCI insight 71 31672932
2021 Mammalian cell proliferation requires noncatalytic functions of O-GlcNAc transferase. Proceedings of the National Academy of Sciences of the United States of America 66 33419956
2001 Nucleocytoplasmic O-glycosylation: O-GlcNAc and functional proteomics. Biochimie 65 11522385
2017 Nutrient-driven O-GlcNAc in proteostasis and neurodegeneration. Journal of neurochemistry 64 29049853
2014 Functional O-GlcNAc modifications: implications in molecular regulation and pathophysiology. Critical reviews in biochemistry and molecular biology 63 24524620
2016 O-GlcNAc transferase inhibitors: current tools and future challenges. Biochemical Society transactions 61 26862193
2019 O-GlcNAc Modification Protects against Protein Misfolding and Aggregation in Neurodegenerative Disease. ACS chemical neuroscience 60 30985105
2020 OGT suppresses S6K1-mediated macrophage inflammation and metabolic disturbance. Proceedings of the National Academy of Sciences of the United States of America 56 32601203
2014 The making of a sweet modification: structure and function of O-GlcNAc transferase. The Journal of biological chemistry 55 25336649
2016 Schwann Cell O-GlcNAc Glycosylation Is Required for Myelin Maintenance and Axon Integrity. The Journal of neuroscience : the official journal of the Society for Neuroscience 54 27629714
2018 O-GlcNAc: A Sweetheart of the Cell Cycle and DNA Damage Response. Frontiers in endocrinology 52 30105004
2014 The role of O-GlcNAc signaling in the pathogenesis of diabetic retinopathy. Proteomics. Clinical applications 52 24550151
2021 O-GlcNAc modified-TIP60/KAT5 is required for PCK1 deficiency-induced HCC metastasis. Oncogene 51 34650217
2022 Integration of O-GlcNAc into Stress Response Pathways. Cells 50 36359905
2018 Functional crosstalk among oxidative stress and O-GlcNAc signaling pathways. Glycobiology 50 29548027
2017 O-GlcNAc Transferase Is Essential for Sensory Neuron Survival and Maintenance. The Journal of neuroscience : the official journal of the Society for Neuroscience 49 28115479
2021 Tools, tactics and objectives to interrogate cellular roles of O-GlcNAc in disease. Nature chemical biology 48 34934185
2014 O-GlcNAcase: promiscuous hexosaminidase or key regulator of O-GlcNAc signaling? The Journal of biological chemistry 48 25336650
2023 Understanding and exploiting the roles of O-GlcNAc in neurodegenerative diseases. The Journal of biological chemistry 40 37918804
2021 Blocked O-GlcNAc cycling alters mitochondrial morphology, function, and mass. Scientific reports 39 34764359
2005 O-GlcNAc modification of nucleocytoplasmic proteins and diabetes. Medical molecular morphology 39 15944815
2024 The OGT-c-Myc-PDK2 axis rewires the TCA cycle and promotes colorectal tumor growth. Cell death and differentiation 38 38778217
2021 Monitoring and modulating O-GlcNAcylation: assays and inhibitors of O-GlcNAc processing enzymes. Current opinion in structural biology 37 33535148
2013 Tools for probing and perturbing O-GlcNAc in cells and in vivo. Current opinion in chemical biology 37 23906602
2020 The O-GlcNAc Modification on Kinases. ACS chemical biology 36 32155042
2019 Structure and function of extracellular O-GlcNAc. Current opinion in structural biology 36 30669087
2018 O-GlcNAc homeostasis contributes to cell fate decisions during hematopoiesis. The Journal of biological chemistry 35 30523150
2017 O-GlcNAc cycling and the regulation of nucleocytoplasmic dynamics. Biochemical Society transactions 35 28408483
2022 Thermal Proteome Profiling Reveals the O-GlcNAc-Dependent Meltome. Journal of the American Chemical Society 34 35230102
2017 OGT: a short overview of an enzyme standing out from usual glycosyltransferases. Biochemical Society transactions 34 28408476
2023 OGT controls mammalian cell viability by regulating the proteasome/mTOR/ mitochondrial axis. Proceedings of the National Academy of Sciences of the United States of America 33 36626549
2022 Specificity of oligonucleotide gene therapy (OGT) agents. Theranostics 32 36276652
2021 O-GlcNAc modification mediates aquaporin 3 to coordinate endometrial cell glycolysis and affects embryo implantation. Journal of advanced research 32 35499042
2023 Cryo-EM structure of human O-GlcNAcylation enzyme pair OGT-OGA complex. Nature communications 31 37907462
2020 Specific O-GlcNAc modification at Ser-615 modulates eNOS function. Redox biology 30 32863226
2018 Thio-Linked UDP-Peptide Conjugates as O-GlcNAc Transferase Inhibitors. Bioconjugate chemistry 30 29723473
2018 O-GlcNAc cycling in the developing, adult and geriatric brain. Journal of bioenergetics and biomembranes 30 29790000
2022 OGT as potential novel target: Structure, function and inhibitors. Chemico-biological interactions 29 35288161
2021 O-GlcNAc Transferase - An Auxiliary Factor or a Full-blown Oncogene? Molecular cancer research : MCR 29 33472950
2020 O-GlcNAc: Regulator of Signaling and Epigenetics Linked to X-linked Intellectual Disability. Frontiers in genetics 29 33329753
2024 OGT and OGA: Sweet guardians of the genome. The Journal of biological chemistry 28 38447797
2020 O-GlcNAc stabilizes SMAD4 by inhibiting GSK-3β-mediated proteasomal degradation. Scientific reports 28 33199824
2019 O-GlcNAc Transferase Inhibition Differentially Affects Breast Cancer Subtypes. Scientific reports 28 30952976
2020 The Emerging Role of Galectins and O-GlcNAc Homeostasis in Processes of Cellular Differentiation. Cells 27 32731422
2020 SIRT1 regulates O-GlcNAcylation of tau through OGT. Aging 26 32310828
2017 Functional significance of O-GlcNAc modification in regulating neuronal properties. Pharmacological research 25 29223644
2022 A nexus of lipid and O-Glcnac metabolism in physiology and disease. Frontiers in endocrinology 24 36111295
2021 OGT Regulates Mitochondrial Biogenesis and Function via Diabetes Susceptibility Gene Pdx1. Diabetes 24 34462257
2017 O-GlcNAc-Dependent Regulation of Progesterone Receptor Function in Breast Cancer. Hormones & cancer 24 28929346
2021 OGT Protein Interaction Network (OGT-PIN): A Curated Database of Experimentally Identified Interaction Proteins of OGT. International journal of molecular sciences 22 34502531
2015 Distinct OGT-Binding Sites Promote HCF-1 Cleavage. PloS one 22 26305326
2014 The potential role of O-GlcNAc modification in cancer epigenetics. Cellular & molecular biology letters 22 25141978
2018 OGT (O-GlcNAc Transferase) Selectively Modifies Multiple Residues Unique to Lamin A. Cells 21 29772801
2009 O-GlcNAc modification and the tauopathies: insights from chemical biology. Current Alzheimer research 21 19874270
2023 Glycophagy mediated glucose-induced changes of hepatic glycogen metabolism via OGT1-AKT1-FOXO1Ser238 pathway. The Journal of nutritional biochemistry 20 36990368
2023 O-GlcNAc Dynamics: The Sweet Side of Protein Trafficking Regulation in Mammalian Cells. Cells 20 37408229
2023 O-GlcNAc has crosstalk with ADP-ribosylation via PARG. The Journal of biological chemistry 20 37858678
2018 'O-GlcNAc Code' Mediated Biological Functions of Downstream Proteins. Molecules (Basel, Switzerland) 20 30082668
2017 "Nutrient-sensing" and self-renewal: O-GlcNAc in a new role. Journal of bioenergetics and biomembranes 20 29204729
2016 O-GlcNAc-ylation in the Nuclear Pore Complex. Cellular and molecular bioengineering 20 28638491
2021 O-GlcNAc modification regulates MTA1 transcriptional activity during breast cancer cell genotoxic adaptation. Biochimica et biophysica acta. General subjects 19 34019948
2018 O-GlcNAc: a novel regulator of immunometabolism. Journal of bioenergetics and biomembranes 19 29404877
2018 T cell development and the physiological role of O-GlcNAc. FEBS letters 19 29904918
2022 O-GlcNAc transferase contributes to sex-specific placental deregulation in gestational diabetes. Placenta 18 36442303
2021 O-linked N-acetylglucosamine transferase (OGT) regulates pancreatic α-cell function in mice. The Journal of biological chemistry 18 33460647

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