2.6.1.16 Adenocarcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29760045&form=6&db=m GFPT2-Expressing Cancer-Associated Fibroblasts Mediate Metabolic Reprogramming in Human Lung Adenocarcinoma. unassigned - 2.6.1.16 Adenocarcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33517899&form=6&db=m High GFPT1 expression predicts unfavorable outcomes in patients with resectable pancreatic ductal adenocarcinoma. causal interaction,diagnostic usage,ongoing research,unassigned 4,4,3,0 2.6.1.16 Adenoviridae Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11679416&form=6&db=m A novel variant of glutamine: fructose-6-phosphate amidotransferase-1 (GFAT1) mRNA is selectively expressed in striated muscle. ongoing research,unassigned 2,0 2.6.1.16 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26715276&form=6&db=m Altered glycometabolism affects both clinical features and prognosis of triple-negative and neoadjuvant chemotherapy-treated breast cancer. causal interaction,diagnostic usage,ongoing research,unassigned 3,4,1,0 2.6.1.16 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32905539&form=6&db=m GFPT2 promotes metastasis and forms a positive feedback loop with p65 in colorectal cancer. causal interaction,therapeutic application,unassigned 3,1,0 2.6.1.16 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=445481&form=6&db=m Characterization of rat hepatoma glucosamine 6-phosphate synthase and its relation to liver and fetal forms. diagnostic usage,ongoing research,unassigned 2,4,0 2.6.1.16 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=4368527&form=6&db=m Comparison of the properties of glucosaminephosphate isomerase (glutamine-forming) from rat liver and a hepatoma. ongoing research,unassigned 4,0 2.6.1.16 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25672227&form=6&db=m The metabolic responses to hepatitis B virus infection shed new light on pathogenesis and targets for treatment. diagnostic usage,unassigned 1,0 2.6.1.16 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28186970&form=6&db=m High expression of GFAT1 predicts unfavorable prognosis in patients with hepatocellular carcinoma. causal interaction,diagnostic usage,unassigned 4,4,0 2.6.1.16 Cardiomegaly http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32286306&form=6&db=m Chronic activation of hexosamine biosynthesis in the heart triggers pathological cardiac remodeling. causal interaction,unassigned 4,0 2.6.1.16 choline o-acetyltransferase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29395675&form=6&db=m Congenital myasthenic syndromes in Turkey: Clinical clues and prognosis with long term follow-up. causal interaction,unassigned 4,0 2.6.1.16 Diabetes Complications http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10198162&form=6&db=m cDNA cloning and mapping of a novel subtype of glutamine:fructose-6-phosphate amidotransferase (GFAT2) in human and mouse. causal interaction,unassigned 1,0 2.6.1.16 Diabetes Complications http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11587069&form=6&db=m Identification of GFAT1-L, a novel splice variant of human glutamine: fructose-6-phosphate amidotransferase (GFAT1) that is expressed abundantly in skeletal muscle. ongoing research,therapeutic application,unassigned 1,1,0 2.6.1.16 Diabetes Complications http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17379537&form=6&db=m Expression and purification of active human internal His(6)-tagged L-glutamine: D-Fructose-6P amidotransferase I. ongoing research,unassigned 2,0 2.6.1.16 Diabetes Mellitus, Type 2 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8593934&form=6&db=m Increased glutamine:fructose-6-phosphate amidotransferase activity in skeletal muscle of patients with NIDDM. causal interaction,unassigned 1,0 2.6.1.16 Diabetes Mellitus, Type 2 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8636435&form=6&db=m Glutamine:fructose-6-phosphate amidotransferase activity in cultured human skeletal muscle cells: relationship to glucose disposal rate in control and non-insulin-dependent diabetes mellitus subjects and regulation by glucose and insulin. ongoing research,unassigned 4,0 2.6.1.16 Diabetes Mellitus, Type 2 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11902440&form=6&db=m From Lobry de Bruyn to enzyme-catalyzed ammonia channelling: molecular studies of D-glucosamine-6P synthase. therapeutic application,unassigned 1,0 2.6.1.16 Diabetes Mellitus, Type 2 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14764791&form=6&db=m Common variants in glutamine:fructose-6-phosphate amidotransferase 2 (GFPT2) gene are associated with type 2 diabetes, diabetic nephropathy, and increased GFPT2 mRNA levels. causal interaction,unassigned 3,0 2.6.1.16 Diabetes Mellitus, Type 2 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17024311&form=6&db=m Effect of +36T>C in intron 1 on the glutamine: fructose-6-phosphate amidotransferase 1 gene and its contribution to type 2 diabetes in different populations. diagnostic usage,ongoing research,therapeutic application,unassigned 3,4,1,0 2.6.1.16 Diabetes Mellitus, Type 2 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17379537&form=6&db=m Expression and purification of active human internal His(6)-tagged L-glutamine: D-Fructose-6P amidotransferase I. ongoing research,unassigned 2,0 2.6.1.16 Diabetes Mellitus, Type 2 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17574229&form=6&db=m Glutamine fructose-6-phosphate amidotransferase (GFAT) gene expression and activity in patients with type 2 diabetes: inter-relationships with hyperglycaemia and oxidative stress. causal interaction,ongoing research,therapeutic application,unassigned 1,3,1,0 2.6.1.16 Diabetes Mellitus, Type 2 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19059404&form=6&db=m Structural analysis of human glutamine:fructose-6-phosphate amidotransferase, a key regulator in type 2 diabetes. ongoing research,unassigned 2,0 2.6.1.16 Diabetes Mellitus, Type 2 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23767808&form=6&db=m Glutamine: fructose-6-phosphate amidotransferase (GFAT): homology modelling and designing of new inhibitors using pharmacophore and docking based hierarchical virtual screening protocol. unassigned - 2.6.1.16 Diabetic Angiopathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12802498&form=6&db=m Glutamine:fructose-6-phosphate aminotransferase enzyme activity is necessary for the induction of TGF-beta1 and fibronectin expression in mesangial cells. therapeutic application,unassigned 1,0 2.6.1.16 Diabetic Nephropathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10997922&form=6&db=m Overexpression of GFAT activates PAI-1 promoter in mesangial cells. unassigned - 2.6.1.16 Diabetic Nephropathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12802498&form=6&db=m Glutamine:fructose-6-phosphate aminotransferase enzyme activity is necessary for the induction of TGF-beta1 and fibronectin expression in mesangial cells. therapeutic application,unassigned 1,0 2.6.1.16 Diabetic Nephropathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14764791&form=6&db=m Common variants in glutamine:fructose-6-phosphate amidotransferase 2 (GFPT2) gene are associated with type 2 diabetes, diabetic nephropathy, and increased GFPT2 mRNA levels. causal interaction,unassigned 3,0 2.6.1.16 Diabetic Nephropathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14988277&form=6&db=m Scrutiny of the glutamine-fructose-6-phosphate transaminase 1 (GFPT1) locus reveals conserved haplotype block structure not associated with diabetic nephropathy. causal interaction,therapeutic application,unassigned 3,1,0 2.6.1.16 Diabetic Nephropathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15308130&form=6&db=m Molecular screening of the human glutamine-fructose-6-phosphate amidotransferase 1 (GFPT1) gene and association studies with diabetes and diabetic nephropathy. causal interaction,diagnostic usage,ongoing research,unassigned 3,1,2,0 2.6.1.16 Esophageal Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32229685&form=6&db=m LncRNA ELFN1-AS1 promotes esophageal cancer progression by up-regulating GFPT1 via sponging miR-183-3p. ongoing research,unassigned 1,0 2.6.1.16 Glioblastoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30771196&form=6&db=m Mammalian Target of Rapamycin 2 (MTOR2) and C-MYC Modulate Glucosamine-6-Phosphate Synthesis in Glioblastoma (GBM) Cells Through Glutamine: Fructose-6-Phosphate Aminotransferase 1 (GFAT1). causal interaction,ongoing research,unassigned 4,1,0 2.6.1.16 Glioblastoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31414301&form=6&db=m Correction to: Mammalian Target of Rapamycin 2 (MTOR2) and C-MYC Modulate Glucosamine-6-Phosphate Synthesis in Glioblastoma (GBM) Cells Through Glutamine: Fructose-6-Phosphate Aminotransferase 1 (GFAT1). ongoing research,unassigned 1,0 2.6.1.16 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30771196&form=6&db=m Mammalian Target of Rapamycin 2 (MTOR2) and C-MYC Modulate Glucosamine-6-Phosphate Synthesis in Glioblastoma (GBM) Cells Through Glutamine: Fructose-6-Phosphate Aminotransferase 1 (GFAT1). causal interaction,ongoing research,unassigned 4,1,0 2.6.1.16 Glucose Intolerance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11118009&form=6&db=m Overexpression of glutamine: fructose-6-phosphate amidotransferase in the liver of transgenic mice results in enhanced glycogen storage, hyperlipidemia, obesity, and impaired glucose tolerance. causal interaction,ongoing research,unassigned 3,1,0 2.6.1.16 glutamine-fructose-6-phosphate transaminase (isomerizing) deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29395675&form=6&db=m Congenital myasthenic syndromes in Turkey: Clinical clues and prognosis with long term follow-up. causal interaction,unassigned 4,0 2.6.1.16 glutamine-fructose-6-phosphate transaminase (isomerizing) deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29905857&form=6&db=m GFPT1 deficiency in muscle leads to myasthenia and myopathy in mice. causal interaction,unassigned 2,0 2.6.1.16 glutamine-fructose-6-phosphate transaminase (isomerizing) deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32286306&form=6&db=m Chronic activation of hexosamine biosynthesis in the heart triggers pathological cardiac remodeling. causal interaction,unassigned 4,0 2.6.1.16 glutamine-fructose-6-phosphate transaminase (isomerizing) deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32615907&form=6&db=m Drosophila GFAT1 and GFAT2 enzymes encode obligate developmental functions. unassigned - 2.6.1.16 Glycogen Storage Disease Type II http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26501342&form=6&db=m Global N-linked Glycosylation is Not Significantly Impaired in Myoblasts in Congenital Myasthenic Syndromes Caused by Defective Glutamine-Fructose-6-Phosphate Transaminase 1 (GFPT1). causal interaction,ongoing research,therapeutic application,unassigned 1,2,1,0 2.6.1.16 Hyperglycemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10997922&form=6&db=m Overexpression of GFAT activates PAI-1 promoter in mesangial cells. unassigned - 2.6.1.16 Hyperglycemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15326559&form=6&db=m Glucose catabolic gene mRNA levels in skeletal muscle exhibit non-coordinate expression in hyperglycemic mice. diagnostic usage,ongoing research,unassigned 3,4,0 2.6.1.16 Hyperglycemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19136606&form=6&db=m The hexosamine biosynthesis inhibitor azaserine prevents endothelial inflammation and dysfunction under hyperglycemic condition through antioxidant effects. therapeutic application,unassigned 1,0 2.6.1.16 Hyperglycemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28582574&form=6&db=m A Genetic Model to Study Increased Hexosamine Biosynthetic Flux. therapeutic application,unassigned 1,0 2.6.1.16 Hyperlipidemias http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11118009&form=6&db=m Overexpression of glutamine: fructose-6-phosphate amidotransferase in the liver of transgenic mice results in enhanced glycogen storage, hyperlipidemia, obesity, and impaired glucose tolerance. causal interaction,ongoing research,unassigned 3,1,0 2.6.1.16 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26770025&form=6&db=m Molecular docking based screening of G6PS with 1, 5 Benzothiazepine derivates for a potential inhibitor. therapeutic application,unassigned 1,0 2.6.1.16 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1460020&form=6&db=m Molecular cloning, cDNA sequence, and bacterial expression of human glutamine:fructose-6-phosphate amidotransferase. causal interaction,unassigned 4,0 2.6.1.16 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1743436&form=6&db=m New insights into the metabolic regulation of insulin action and insulin resistance: role of glucose and amino acids. causal interaction,unassigned 1,0 2.6.1.16 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8349040&form=6&db=m Regulation of insulin-stimulated glycogen synthase activity by overexpression of glutamine: fructose-6-phosphate amidotransferase in rat-1 fibroblasts. ongoing research,unassigned 4,0 2.6.1.16 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8770864&form=6&db=m Overexpression of glutamine:fructose-6-phosphate amidotransferase in transgenic mice leads to insulin resistance. ongoing research,unassigned 4,0 2.6.1.16 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8798515&form=6&db=m Differential effects of GLUT1 or GLUT4 overexpression on hexosamine biosynthesis by muscles of transgenic mice. unassigned - 2.6.1.16 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10067838&form=6&db=m Mechanism of hexosamine-induced insulin resistance in transgenic mice overexpressing glutamine:fructose-6-phosphate amidotransferase: decreased glucose transporter GLUT4 translocation and reversal by treatment with thiazolidinedione. causal interaction,therapeutic application,unassigned 1,3,0 2.6.1.16 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11167021&form=6&db=m Cloning and characterization of mouse glutamine:fructose-6-phosphate amidotransferase 2 gene promoter. causal interaction,unassigned 1,0 2.6.1.16 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11587069&form=6&db=m Identification of GFAT1-L, a novel splice variant of human glutamine: fructose-6-phosphate amidotransferase (GFAT1) that is expressed abundantly in skeletal muscle. ongoing research,therapeutic application,unassigned 1,1,0 2.6.1.16 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12044898&form=6&db=m Glucosamine-6-phosphate synthase--the multi-facets enzyme. unassigned - 2.6.1.16 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14684615&form=6&db=m Activation of the hexosamine signaling pathway in adipose tissue results in decreased serum adiponectin and skeletal muscle insulin resistance. ongoing research,unassigned 2,0 2.6.1.16 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15595739&form=6&db=m Molecular therapeutic target for type-2 diabetes. therapeutic application,unassigned 1,0 2.6.1.16 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16555472&form=6&db=m Effect of sucrose and saturated-fat diets on mRNA levels of genes limiting muscle fatty acid and glucose supply in rats. causal interaction,unassigned 2,0 2.6.1.16 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17574229&form=6&db=m Glutamine fructose-6-phosphate amidotransferase (GFAT) gene expression and activity in patients with type 2 diabetes: inter-relationships with hyperglycaemia and oxidative stress. causal interaction,ongoing research,therapeutic application,unassigned 1,3,1,0 2.6.1.16 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19036880&form=6&db=m Hexosamine biosynthesis pathway flux contributes to insulin resistance via altering membrane phosphatidylinositol 4,5-bisphosphate and cortical filamentous actin. diagnostic usage,ongoing research,unassigned 1,1,0 2.6.1.16 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19757168&form=6&db=m Molecular characterization, chromosomal location, alternative splicing and polymorphism of porcine GFAT1 gene. unassigned - 2.6.1.16 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20658157&form=6&db=m Increased hexosamine pathway flux and high fat feeding are not additive in inducing insulin resistance: evidence for a shared pathway. unassigned - 2.6.1.16 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23050969&form=6&db=m Select nutrients, progesterone, and interferon tau affect conceptus metabolism and development. ongoing research,unassigned 2,0 2.6.1.16 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28582574&form=6&db=m A Genetic Model to Study Increased Hexosamine Biosynthetic Flux. therapeutic application,unassigned 1,0 2.6.1.16 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33916835&form=6&db=m High-Fat Diet Leads to Reduced Protein O-GlcNAcylation and Mitochondrial Defects Promoting the Development of Alzheimer's Disease Signatures. unassigned - 2.6.1.16 Iron Deficiencies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33430126&form=6&db=m Iron Deficiency Reprograms Phosphorylation Signaling and Reduces O-GlcNAc Pathways in Neuronal Cells. unassigned - 2.6.1.16 Leukemia L1210 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1814130&form=6&db=m The influence of L-norvalyl-N3-4-methoxyfumaroyl-L-2,3-diaminopropanoic acid, an antifungal agent, on mammalian cells in tissue culture. ongoing research,unassigned 2,0 2.6.1.16 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8882734&form=6&db=m Effects of monophosphoryllipid-A on the immunization of mice with keyhole limpet hemocyanin- and muramyldipeptide-ganglioside Gfpt1 conjugates. ongoing research,therapeutic application,unassigned 4,2,0 2.6.1.16 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34270713&form=6&db=m Inhibition of GFAT1 in lung cancer cells destabilizes PD-L1 protein. causal interaction,ongoing research,therapeutic application,unassigned 2,3,4,0 2.6.1.16 Lymphatic Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27509259&form=6&db=m Loss of GFAT1 promotes epithelial-to-mesenchymal transition and predicts unfavorable prognosis in gastric cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,4,4,4 2.6.1.16 Lymphatic Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27996048&form=6&db=m High expression of GFAT1 predicts poor prognosis in patients with pancreatic cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,2,1 2.6.1.16 Malaria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27150044&form=6&db=m Identifying antimalarial compounds targeting dihydrofolate reductase-thymidylate synthase (DHFR-TS) by chemogenomic profiling. ongoing research,therapeutic application,unassigned 2,4,0 2.6.1.16 Malaria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31797898&form=6&db=m Overexpression of the HECT ubiquitin ligase PfUT prolongs the intraerythrocytic cycle and reduces invasion efficiency of Plasmodium falciparum. ongoing research,unassigned 2,0 2.6.1.16 Melanoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26883802&form=6&db=m UDP-sugar substrates of HAS3 regulate its O-GlcNAcylation, intracellular traffic, extracellular shedding and correlate with melanoma progression. causal interaction,ongoing research,unassigned 1,1,0 2.6.1.16 Metabolic Syndrome http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20332082&form=6&db=m Lipogenesis is decreased by grape seed proanthocyanidins according to liver proteomics of rats fed a high fat diet. causal interaction,therapeutic application,unassigned 3,4,0 2.6.1.16 Muscle Weakness http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23569079&form=6&db=m Mutations in GFPT1 that underlie limb-girdle congenital myasthenic syndrome result in reduced cell-surface expression of muscle AChR. causal interaction,unassigned 3,0 2.6.1.16 Muscle Weakness http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29905857&form=6&db=m GFPT1 deficiency in muscle leads to myasthenia and myopathy in mice. causal interaction,unassigned 2,0 2.6.1.16 Muscular Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26501342&form=6&db=m Global N-linked Glycosylation is Not Significantly Impaired in Myoblasts in Congenital Myasthenic Syndromes Caused by Defective Glutamine-Fructose-6-Phosphate Transaminase 1 (GFPT1). causal interaction,ongoing research,therapeutic application,unassigned 1,2,1,0 2.6.1.16 Muscular Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27941137&form=6&db=m Tubular Aggregates and Cylindrical Spirals Have Distinct Immunohistochemical Signatures. unassigned - 2.6.1.16 Muscular Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29905857&form=6&db=m GFPT1 deficiency in muscle leads to myasthenia and myopathy in mice. causal interaction,unassigned 2,0 2.6.1.16 Muscular Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31255525&form=6&db=m Novel compound heterozygous GFPT1 mutations in a family with limb-girdle myasthenia with tubular aggregates. causal interaction,therapeutic application,unassigned 3,3,0 2.6.1.16 Muscular Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31449669&form=6&db=m Trouble at the junction: When myopathy and myasthenia overlap. causal interaction,unassigned 2,0 2.6.1.16 Muscular Dystrophies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26501342&form=6&db=m Global N-linked Glycosylation is Not Significantly Impaired in Myoblasts in Congenital Myasthenic Syndromes Caused by Defective Glutamine-Fructose-6-Phosphate Transaminase 1 (GFPT1). causal interaction,ongoing research,therapeutic application,unassigned 1,2,1,0 2.6.1.16 Muscular Dystrophies, Limb-Girdle http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26501342&form=6&db=m Global N-linked Glycosylation is Not Significantly Impaired in Myoblasts in Congenital Myasthenic Syndromes Caused by Defective Glutamine-Fructose-6-Phosphate Transaminase 1 (GFPT1). causal interaction,ongoing research,therapeutic application,unassigned 1,2,1,0 2.6.1.16 Myasthenic Syndromes, Congenital http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21975507&form=6&db=m Congenital myasthenic syndrome with tubular aggregates caused by GFPT1 mutations. causal interaction,diagnostic usage,unassigned 3,3,0 2.6.1.16 Myasthenic Syndromes, Congenital http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22742743&form=6&db=m Mutations in DPAGT1 cause a limb-girdle congenital myasthenic syndrome with tubular aggregates. causal interaction,unassigned 4,0 2.6.1.16 Myasthenic Syndromes, Congenital http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22987706&form=6&db=m Limb-girdle myasthenia with tubular aggregates associated with novel GFPT1 mutations. causal interaction,unassigned 3,0 2.6.1.16 Myasthenic Syndromes, Congenital http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23569079&form=6&db=m Mutations in GFPT1 that underlie limb-girdle congenital myasthenic syndrome result in reduced cell-surface expression of muscle AChR. causal interaction,unassigned 3,0 2.6.1.16 Myasthenic Syndromes, Congenital http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25765662&form=6&db=m A 3'-UTR mutation creates a microRNA target site in the GFPT1 gene of patients with congenital myasthenic syndrome. causal interaction,therapeutic application,unassigned 3,1,0 2.6.1.16 Myasthenic Syndromes, Congenital http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26501342&form=6&db=m Global N-linked Glycosylation is Not Significantly Impaired in Myoblasts in Congenital Myasthenic Syndromes Caused by Defective Glutamine-Fructose-6-Phosphate Transaminase 1 (GFPT1). causal interaction,ongoing research,therapeutic application,unassigned 1,2,1,0 2.6.1.16 Myasthenic Syndromes, Congenital http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27941137&form=6&db=m Tubular Aggregates and Cylindrical Spirals Have Distinct Immunohistochemical Signatures. unassigned - 2.6.1.16 Myasthenic Syndromes, Congenital http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28712002&form=6&db=m Mutations in GFPT1-related congenital myasthenic syndromes are associated with synaptic morphological defects and underlie a tubular aggregate myopathy with synaptopathy. causal interaction,unassigned 1,0 2.6.1.16 Myasthenic Syndromes, Congenital http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29905857&form=6&db=m GFPT1 deficiency in muscle leads to myasthenia and myopathy in mice. causal interaction,unassigned 2,0 2.6.1.16 Myasthenic Syndromes, Congenital http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30635494&form=6&db=m Leukoencephalopathy due to variants in GFPT1-associated congenital myasthenic syndrome. unassigned - 2.6.1.16 Myasthenic Syndromes, Congenital http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30846217&form=6&db=m Phenotype of a limb-girdle congenital myasthenic syndrome patient carrying a GFPT1 mutation. causal interaction,unassigned 3,0 2.6.1.16 Myasthenic Syndromes, Congenital http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31449669&form=6&db=m Trouble at the junction: When myopathy and myasthenia overlap. causal interaction,unassigned 2,0 2.6.1.16 Myasthenic Syndromes, Congenital http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32754643&form=6&db=m Congenital myasthenic syndrome caused by a frameshift insertion mutation in GFPT1. causal interaction,unassigned 3,0 2.6.1.16 Myasthenic Syndromes, Congenital http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33438142&form=6&db=m Novel compound heterozygous variants in the GFPT1 gene leading to rare limb-girdle congenital myasthenic syndrome with rimmed vacuoles. unassigned - 2.6.1.16 Mycoses http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10910723&form=6&db=m Purification to homogeneity of Candida albicans glucosamine-6-phosphate synthase overexpressed in Escherichia coli. ongoing research,therapeutic application,unassigned 1,3,0 2.6.1.16 Mycoses http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21904431&form=6&db=m Functional co-evolutionary study of glucosamine-6-phosphate synthase in mycoses causing fungi. ongoing research,unassigned 2,0 2.6.1.16 Myocardial Infarction http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22128088&form=6&db=m Cardiac O-GlcNAc signaling is increased in hypertrophy and heart failure. ongoing research,unassigned 2,0 2.6.1.16 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27509259&form=6&db=m Loss of GFAT1 promotes epithelial-to-mesenchymal transition and predicts unfavorable prognosis in gastric cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,4,4,4 2.6.1.16 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27996048&form=6&db=m High expression of GFAT1 predicts poor prognosis in patients with pancreatic cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,2,1 2.6.1.16 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33517899&form=6&db=m High GFPT1 expression predicts unfavorable outcomes in patients with resectable pancreatic ductal adenocarcinoma. causal interaction,diagnostic usage,ongoing research,unassigned 4,4,3,0 2.6.1.16 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=947&form=6&db=m Carcinofetal alterations in glucosamine-6-phosphate synthetase. unassigned - 2.6.1.16 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8882734&form=6&db=m Effects of monophosphoryllipid-A on the immunization of mice with keyhole limpet hemocyanin- and muramyldipeptide-ganglioside Gfpt1 conjugates. ongoing research,therapeutic application,unassigned 4,2,0 2.6.1.16 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26715276&form=6&db=m Altered glycometabolism affects both clinical features and prognosis of triple-negative and neoadjuvant chemotherapy-treated breast cancer. causal interaction,diagnostic usage,ongoing research,unassigned 3,4,1,0 2.6.1.16 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27509259&form=6&db=m Loss of GFAT1 promotes epithelial-to-mesenchymal transition and predicts unfavorable prognosis in gastric cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,4,4,4 2.6.1.16 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27758869&form=6&db=m Hyaluronan Production Regulates Metabolic and Cancer Stem-like Properties of Breast Cancer Cells via Hexosamine Biosynthetic Pathway-coupled HIF-1 Signaling. unassigned - 2.6.1.16 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28186970&form=6&db=m High expression of GFAT1 predicts unfavorable prognosis in patients with hepatocellular carcinoma. causal interaction,diagnostic usage,unassigned 4,4,0 2.6.1.16 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30912436&form=6&db=m Emerging Anticancer Activity of Candidal Glucoseamine-6-Phosphate Synthase Inhibitors upon Nanoparticle-Mediated Delivery. ongoing research,therapeutic application,unassigned 4,1,0 2.6.1.16 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31645543&form=6&db=m Enhanced hexosamine metabolism drives metabolic and signaling networks involving hyaluronan production and O-GlcNAcylation to exacerbate breast cancer. causal interaction,diagnostic usage,unassigned 1,3,0 2.6.1.16 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33517899&form=6&db=m High GFPT1 expression predicts unfavorable outcomes in patients with resectable pancreatic ductal adenocarcinoma. causal interaction,diagnostic usage,ongoing research,unassigned 4,4,3,0 2.6.1.16 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34270713&form=6&db=m Inhibition of GFAT1 in lung cancer cells destabilizes PD-L1 protein. causal interaction,ongoing research,therapeutic application,unassigned 2,3,4,0 2.6.1.16 Neuromuscular Junction Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21975507&form=6&db=m Congenital myasthenic syndrome with tubular aggregates caused by GFPT1 mutations. causal interaction,diagnostic usage,unassigned 3,3,0 2.6.1.16 Obesity http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11118009&form=6&db=m Overexpression of glutamine: fructose-6-phosphate amidotransferase in the liver of transgenic mice results in enhanced glycogen storage, hyperlipidemia, obesity, and impaired glucose tolerance. causal interaction,ongoing research,unassigned 3,1,0 2.6.1.16 Obesity http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15613432&form=6&db=m The -913 G/A glutamine:fructose-6-phosphate aminotransferase gene polymorphism is associated with measures of obesity and intramyocellular lipid content in nondiabetic subjects. causal interaction,unassigned 1,0 2.6.1.16 Pancreatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27996048&form=6&db=m High expression of GFAT1 predicts poor prognosis in patients with pancreatic cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,2,1 2.6.1.16 Pancreatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29753740&form=6&db=m 2-Deoxy-d-glucose increases GFAT1 phosphorylation resulting in endoplasmic reticulum-related apoptosis via disruption of protein N-glycosylation in pancreatic cancer cells. causal interaction,therapeutic application,unassigned 4,2,0 2.6.1.16 Pulmonary Fibrosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6184359&form=6&db=m Elevation of glucosamine 6-phosphate synthetase activity in bleomycin-induced pulmonary fibrosis in hamsters. causal interaction,unassigned 4,0 2.6.1.16 Pulmonary Fibrosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6195141&form=6&db=m Peplomycin sulfate and pulmonary fibrosis: hydroxyproline, uronic acid, proline hydroxylase and glucosamine 6-phosphate synthetase in lungs of hamsters treated with peplomycin. therapeutic application,unassigned 1,0 2.6.1.16 Small Cell Lung Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8882734&form=6&db=m Effects of monophosphoryllipid-A on the immunization of mice with keyhole limpet hemocyanin- and muramyldipeptide-ganglioside Gfpt1 conjugates. ongoing research,therapeutic application,unassigned 4,2,0 2.6.1.16 Starvation http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30201609&form=6&db=m mTORC2 modulates the amplitude and duration of GFAT1 Ser243 phosphorylation to maintain flux through the hexosamine pathway during starvation. therapeutic application,unassigned 1,0 2.6.1.16 Stomach Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27509259&form=6&db=m Loss of GFAT1 promotes epithelial-to-mesenchymal transition and predicts unfavorable prognosis in gastric cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,4,4,4 2.6.1.16 Stomach Ulcer http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=5679467&form=6&db=m Aminosugars in cases of gastric ulcers. II. The activity of L-glutamine: D-fructose-6-phosphate aminotransferase (E. C. 2.6.1.16) in human gastric mucous membrane. diagnostic usage,ongoing research,unassigned 1,2,0 2.6.1.16 Triple Negative Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26715276&form=6&db=m Altered glycometabolism affects both clinical features and prognosis of triple-negative and neoadjuvant chemotherapy-treated breast cancer. causal interaction,diagnostic usage,ongoing research,unassigned 3,4,1,0