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Disease on EC 2.4.1.222 - O-fucosylpeptide 3-beta-N-acetylglucosaminyltransferase

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DISEASE
TITLE OF PUBLICATION
LINK TO PUBMED
Abortion, Spontaneous
Altered ?1,6-GlcNAc and bisecting GlcNAc-branched N-glycan on integrin ?1 are associated with early spontaneous miscarriage in humans.
Adenocarcinoma
Lunatic Fringe is a potent tumor suppressor in Kras-initiated pancreatic cancer.
The Notch pathway in ovarian carcinomas and adenomas.
Adenoma
Manic Fringe deficiency imposes Jagged1 addiction to intestinal tumor cells.
The Notch pathway in ovarian carcinomas and adenomas.
alpha-1,6-mannosyl-glycoprotein 2-beta-n-acetylglucosaminyltransferase deficiency
Carbohydrate-deficient glycoprotein syndrome type II. An autosomal recessive N-acetylglucosaminyltransferase II deficiency different from typical hereditary erythroblastic multinuclearity, with a positive acidified-serum lysis test (HEMPAS).
Anemia
Primary defect of congenital dyserythropoietic anemia type II. Failure in glycosylation of erythrocyte lactosaminoglycan proteins caused by lowered N-acetylglucosaminyltransferase II.
Anemia, Dyserythropoietic, Congenital
Primary defect of congenital dyserythropoietic anemia type II. Failure in glycosylation of erythrocyte lactosaminoglycan proteins caused by lowered N-acetylglucosaminyltransferase II.
Brain Neoplasms
Glycosyltransferase activities in human meningiomas. Preliminary results.
Breast Neoplasms
B3GNT3 overexpression promotes tumor progression and inhibits infiltration of CD8+ T cells in pancreatic cancer.
Inhibition of a specific N-glycosylation activity results in attenuation of breast carcinoma cell invasiveness-related phenotypes: inhibition of epidermal growth factor-induced dephosphorylation of focal adhesion kinase.
Lunatic Fringe and p53 Cooperatively Suppress Mesenchymal Stem-Like Breast Cancer.
Lunatic fringe deficiency cooperates with the Met/Caveolin gene amplicon to induce basal-like breast cancer.
Manic fringe promotes a claudin-low breast cancer phenotype through notch-mediated PIK3CG induction.
CADASIL
CADASIL mutations impair Notch3 glycosylation by Fringe.
Lunatic fringe promotes the aggregation of CADASIL NOTCH3 mutant proteins.
Carcinogenesis
Effects of H-ras and v-sis overexpression on N-acetylglucosaminyltransferase V and metastasis-related phenotypes in human hepatocarcinoma cells.
Carcinoma
Changes in N-acetylglucosaminyltransferase III, IV and V in renal cell carcinoma.
Inhibition of a specific N-glycosylation activity results in attenuation of breast carcinoma cell invasiveness-related phenotypes: inhibition of epidermal growth factor-induced dephosphorylation of focal adhesion kinase.
Notch signalling is linked to epidermal cell differentiation level in basal cell carcinoma, psoriasis and wound healing.
Nuclear and stromal expression of Manic fringe in renal cell carcinoma.
Carcinoma, Basal Cell
Notch signalling is linked to epidermal cell differentiation level in basal cell carcinoma, psoriasis and wound healing.
Carcinoma, Hepatocellular
Distribution of glycosyltransferases among Golgi apparatus subfractions from liver and hepatomas of the rat.
Studies on UDP-N-acetylglucosamine : alpha-mannoside beta-N-acetylglucosaminyltransferase of rat liver and hepatomas.
Carcinoma, Non-Small-Cell Lung
Downregulation of N-Acetylglucosaminyltransferase GCNT3 by miR-302b-3p Decreases Non-Small Cell Lung Cancer (NSCLC) Cell Proliferation, Migration and Invasion.
Carcinoma, Renal Cell
Changes in N-acetylglucosaminyltransferase III, IV and V in renal cell carcinoma.
Nuclear and stromal expression of Manic fringe in renal cell carcinoma.
Cardiomyopathies
Reduced myocyte complex N-glycosylation causes dilated cardiomyopathy.
Choriocarcinoma
Abnormal biantennary sugar chains are expressed in human chorionic gonadotropin produced in the choriocarcinoma cell line, JEG-3.
Colonic Neoplasms
A novel beta1,3-N-acetylglucosaminyltransferase (beta3Gn-T8), which synthesizes poly-N-acetyllactosamine, is dramatically upregulated in colon cancer.
Congenital Disorders of Glycosylation
Carbohydrate-deficient glycoprotein syndrome type II. An autosomal recessive N-acetylglucosaminyltransferase II deficiency different from typical hereditary erythroblastic multinuclearity, with a positive acidified-serum lysis test (HEMPAS).
Diphtheria
Biochemical studies of inositol N-acetylglucosaminyltransferase involved in mycothiol biosynthesis in Corynebacterium diphtheria.
Dysostoses
Disruption of the somitic molecular clock causes abnormal vertebral segmentation.
Mutation of the LUNATIC FRINGE gene in humans causes spondylocostal dysostosis with a severe vertebral phenotype.
Glioma
Glioma cell fate decisions mediated by Dll1-Jag1-Fringe in Notch1 signaling pathway.
Infections
Excess lunatic fringe causes cranial neural crest over-proliferation.
Infertility
A deficiency of lunatic fringe is associated with cystic dilation of the rete testis.
Infertility, Female
A loss of lunatic fringe is associated with female infertility.
Liver Neoplasms
mRNA expression of three glycosyltransferases in human hepatoma tissues.
Lung Neoplasms
Downregulation of N-Acetylglucosaminyltransferase GCNT3 by miR-302b-3p Decreases Non-Small Cell Lung Cancer (NSCLC) Cell Proliferation, Migration and Invasion.
Manic fringe inhibits tumor growth by suppressing Notch3 degradation in lung cancer.
Lymphoma
A mouse lymphoma cell line resistant to the leukoagglutinating lectin from Phaseolus vulgaris is deficient in UDP-GlcNAc: alpha-D-mannoside beta 1,6 N-acetylglucosaminyltransferase.
Malaria
N-acetylglucosaminyltransferase V-deficiency increases susceptibility to murine malaria.
Melanoma
Aberrant glycosylation of E-cadherin enhances cell-cell binding to suppress metastasis.
Comparative genomics reveals that loss of lunatic fringe (LFNG) promotes melanoma metastasis.
Melanoma-associated glycosyltransferase GCNT2 as an emerging biomarker and therapeutic target.
miR-146a Exerts Differential Effects on Melanoma Growth and Metastatization.
[Suppression of lung metastasis of B16 mouse melanoma cells by introduction of N-acetylglucosaminyltransferase III gene]
Meningioma
Glycosyltransferase activities in human meningiomas. Preliminary results.
Multiple Sclerosis
Activity levels of a beta1,6 N-acetylglucosaminyltransferase in lymphomonocytes from multiple sclerosis patients.
Muscular Dystrophies
Biochemical and biophysical changes underlie the mechanisms of basement membrane disruptions in a mouse model of dystroglycanopathy.
Retinal ectopias and mechanically weakened basement membrane in a mouse model of muscle-eye-brain (MEB) disease congenital muscular dystrophy.
Neoplasm Metastasis
Aberrant glycosylation of E-cadherin enhances cell-cell binding to suppress metastasis.
Comparative genomics reveals that loss of lunatic fringe (LFNG) promotes melanoma metastasis.
Effects of H-ras and v-sis overexpression on N-acetylglucosaminyltransferase V and metastasis-related phenotypes in human hepatocarcinoma cells.
Elevated expression of UDP-N-acetylglucosamine: alphamannoside beta1,6 N-acetylglucosaminyltransferase is an early event in hepatocarcinogenesis.
miR-146a Exerts Differential Effects on Melanoma Growth and Metastatization.
Recent progress in the molecular biology of the cloned N-acetylglucosaminyltransferases.
[Suppression of lung metastasis of B16 mouse melanoma cells by introduction of N-acetylglucosaminyltransferase III gene]
Neoplasms
A novel beta1,3-N-acetylglucosaminyltransferase involved in invasion of cancer cells as assayed in vitro.
B3GNT3 overexpression promotes tumor progression and inhibits infiltration of CD8+ T cells in pancreatic cancer.
Biosynthesis of blood group i-active polylactosaminoglycans. Partial purification and properties of an UDP-GlcNAc:N-acetyllactosaminide beta 1----3-N-acetylglucosaminyltransferase from Novikoff tumor cell ascites fluid.
Correlated gene expression between beta-1,4-galactosyltransferase V and N-acetylglucosaminyltransferase V in human cancer cell lines.
Elevated expression of UDP-N-acetylglucosamine: alphamannoside beta1,6 N-acetylglucosaminyltransferase is an early event in hepatocarcinogenesis.
Inflammatory Stress Causes N-Glycan Processing Deficiency in Ocular Autoimmune Disease.
Lunatic Fringe and p53 Cooperatively Suppress Mesenchymal Stem-Like Breast Cancer.
Lunatic Fringe is a potent tumor suppressor in Kras-initiated pancreatic cancer.
Manic Fringe deficiency imposes Jagged1 addiction to intestinal tumor cells.
Manic fringe inhibits tumor growth by suppressing Notch3 degradation in lung cancer.
Novikoff ascites tumor cells contain N-acetyllactosaminide beta 1 leads to 3 and beta 1 leads to 6 N-acetylglucosaminyltransferase activity.
Papillomavirus-mediated neoplastic progression is associated with reciprocal changes in JAGGED1 and manic fringe expression linked to notch activation.
Recent progress in the molecular biology of the cloned N-acetylglucosaminyltransferases.
The metastatic potential of rat prostate tumor variant R3327-MatLyLu is correlated with an increased activity of N-acetylglucosaminyl transferase III and V.
Tumor-Suppressive Activity of Lunatic Fringe in Prostate through Differential Modulation of Notch Receptor Activation.
o-fucosylpeptide 3-beta-n-acetylglucosaminyltransferase deficiency
Lunatic fringe deficiency cooperates with the Met/Caveolin gene amplicon to induce basal-like breast cancer.
Manic Fringe deficiency imposes Jagged1 addiction to intestinal tumor cells.
Pancreatic Neoplasms
Lunatic Fringe is a potent tumor suppressor in Kras-initiated pancreatic cancer.
Pemphigoid, Bullous
Inflammatory Stress Causes N-Glycan Processing Deficiency in Ocular Autoimmune Disease.
Psoriasis
Notch signalling is linked to epidermal cell differentiation level in basal cell carcinoma, psoriasis and wound healing.
Scoliosis
Mutations in the notch pathway alter the patterning of multifidus.
Tooth Abnormalities
Lunatic fringe, FGF, and BMP regulate the Notch pathway during epithelial morphogenesis of teeth.
Vesicular Stomatitis
Growth of enveloped RNA viruses in a line of chinese hamster ovary cells with deficient N-acetylglucosaminyltransferase activity.
Virus Diseases
[Mitochondrial N-acetylglucosaminyl transferase connected with viral infection]
Walker-Warburg Syndrome
Loss-of-function of an N-acetylglucosaminyltransferase, POMGnT1, in muscle-eye-brain disease.