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Disease on EC 2.3.1.22 - 2-acylglycerol O-acyltransferase

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DISEASE
TITLE OF PUBLICATION
LINK TO PUBMED
2-acylglycerol o-acyltransferase deficiency
Adult-onset deficiency of acyl CoA:monoacylglycerol acyltransferase 2 protects mice from diet-induced obesity and glucose intolerance.
Defective Phosphatidylglycerol Remodeling Causes Hepatopathy, Linking Mitochondrial Dysfunction to Hepatosteatosis.
Deficiency of MGAT2 increases energy expenditure without high-fat feeding and protects genetically obese mice from excessive weight gain.
MGAT2 deficiency (CDG-IIa): The Life of J.
MGAT2 deficiency ameliorates high-fat diet-induced obesity and insulin resistance by inhibiting intestinal fat absorption in mice.
MGAT2 deficiency and vertical sleeve gastrectomy have independent metabolic effects in the mouse.
Alzheimer Disease
Delineating Alzheimer's disease progression with MGAT3, a biomarker for improved prognosis and personalized therapy.
MGAT3 mRNA: A Biomarker for Prognosis and Therapy of Alzheimer's Disease by Vitamin D and Curcuminoids.
Bardet-Biedl Syndrome
Novel variants in women with premature ovarian function decline identified via whole-exome sequencing.
beta-1,4-mannosyl-glycoprotein 4-beta-n-acetylglucosaminyltransferase deficiency
Bisecting GlcNAc modification stabilizes BACE1 protein under oxidative stress conditions.
Breast Neoplasms
Bisected, complex N-glycans and galectins in mouse mammary tumor progression and human breast cancer.
Bisecting N-Acetylglucosamine on EGFR Inhibits Malignant Phenotype of Breast Cancer via Down-Regulation of EGFR/Erk Signaling.
The plasma peptides of breast versus ovarian cancer.
Carcinoma
The glycosyltransferase GnT-III activates Notch signaling and drives stem cell expansion to promote the growth and invasion of ovarian cancer.
Carcinoma, Hepatocellular
MiR-23a transcriptional activated by Runx2 increases metastatic potential of mouse hepatoma cell via directly targeting Mgat3.
The bisecting GlcNAc on N-glycans inhibits growth factor signaling and retards mammary tumor progression.
Carcinoma, Ovarian Epithelial
The glycosyltransferase GnT-III activates Notch signaling and drives stem cell expansion to promote the growth and invasion of ovarian cancer.
Cardiomyopathies
Reduced myocyte complex N-glycosylation causes dilated cardiomyopathy.
Colitis, Ulcerative
Promoter methylation of the MGAT3 and BACH2 genes correlates with the composition of the immunoglobulin G glycome in inflammatory bowel disease.
Congenital Disorders of Glycosylation
Mutations in the MGAT2 gene controlling complex N-glycan synthesis cause carbohydrate-deficient glycoprotein syndrome type II, an autosomal recessive disease with defective brain development.
Congenital, Hereditary, and Neonatal Diseases and Abnormalities
Mice with a homozygous deletion of the Mgat2 gene encoding UDP-N-acetylglucosamine:alpha-6-D-mannoside beta1,2-N-acetylglucosaminyltransferase II: a model for congenital disorder of glycosylation type IIa.
Crohn Disease
Promoter methylation of the MGAT3 and BACH2 genes correlates with the composition of the immunoglobulin G glycome in inflammatory bowel disease.
Demyelinating Diseases
Genetics and the environment converge to dysregulate N-glycosylation in multiple sclerosis.
N-glycan processing deficiency promotes spontaneous inflammatory demyelination and neurodegeneration.
Diabetes Mellitus
Inhibition of MGAT2 modulates fat-induced gut peptide release and fat intake in normal mice and ameliorates obesity and diabetes in ob/ob mice fed on a high-fat diet.
Diabetes Mellitus, Type 1
Family studies of type 1 diabetes reveal additive and epistatic effects between MGAT1 and three other polymorphisms.
Diabetes Mellitus, Type 2
Cell-based assay of MGAT2-driven diacylglycerol synthesis for profiling inhibitors: use of a stable isotope-labeled substrate and high-resolution LC/MS.
Hepatic Monoacylglycerol O-acyltransferase 1 as a Promising Therapeutic Target for Steatosis, Obesity, and Type 2 Diabetes.
Inhibition of MGAT2 modulates fat-induced gut peptide release and fat intake in normal mice and ameliorates obesity and diabetes in ob/ob mice fed on a high-fat diet.
Dyslipidemias
Pharmacological Inhibition of Monoacylglycerol O-Acyltransferase 2 Improves Hyperlipidemia, Obesity, and Diabetes by Change in Intestinal Fat Utilization.
Epilepsy
First demonstration of a functional role for central nervous system betaine/{gamma}-aminobutyric acid transporter (mGAT2) based on synergistic anticonvulsant action among inhibitors of mGAT1 and mGAT2.
First photoswitchable neurotransmitter transporter inhibitor: light-induced control of ?-aminobutyric acid transporter 1 (GAT1) activity in mouse brain.
Generation and screening of oxime libraries addressing the neuronal GABA transporter GAT1.
Synthesis and evaluation of N-substituted nipecotic acid derivatives with an unsymmetrical bis-aromatic residue attached to a vinyl ether spacer as potential GABA uptake inhibitors.
Fabry Disease
Reexpression of HPRT activity following cell fusion with polyethylene glycol.
Fatty Liver
Monoacylglycerol O-acyltransferase 1 is regulated by peroxisome proliferator-activated receptor ? in human hepatocytes and increases lipid accumulation.
Pharmacological Inhibition of Monoacylglycerol O-Acyltransferase 2 Improves Hyperlipidemia, Obesity, and Diabetes by Change in Intestinal Fat Utilization.
Suppression of PPAR?-mediated monoacylglycerol O-acyltransferase 1 expression ameliorates alcoholic hepatic steatosis.
Glioblastoma
N-acetylglucosaminyltransferase I promotes glioma cell proliferation and migration through increasing the stability of the glucose transporter GLUT1.
Glioma
N-acetylglucosaminyltransferase I promotes glioma cell proliferation and migration through increasing the stability of the glucose transporter GLUT1.
Glucose Intolerance
Adult-onset deficiency of acyl CoA:monoacylglycerol acyltransferase 2 protects mice from diet-induced obesity and glucose intolerance.
Intestine-specific deletion of acyl-CoA:monoacylglycerol acyltransferase (MGAT) 2 protects mice from diet-induced obesity and glucose intolerance.
Multiple antisense oligonucleotides targeted against monoacylglycerol acyltransferase 1 (Mogat1) improve glucose metabolism independently of Mogat1.
Heart Failure
Reduced hybrid/complex N-glycosylation disrupts cardiac electrical signaling and calcium handling in a model of dilated cardiomyopathy.
Herpes Zoster
Oocyte-specific deletion of complex and hybrid N-glycans leads to defects in preovulatory follicle and cumulus mass development.
Hyperglycemia
Pharmacological Inhibition of Monoacylglycerol O-Acyltransferase 2 Improves Hyperlipidemia, Obesity, and Diabetes by Change in Intestinal Fat Utilization.
Hyperlipidemias
Pharmacological characterization of a series of aryl-sulfonamide derivatives that potently and selectively inhibit monoacylglycerol acyltransferase 2.
Pharmacological Inhibition of Monoacylglycerol O-Acyltransferase 2 Improves Hyperlipidemia, Obesity, and Diabetes by Change in Intestinal Fat Utilization.
Hypertriglyceridemia
Identification of 12 novel loci that confer susceptibility to early-onset dyslipidemia.
Infections
Genetic engineering of CHO cells for viral resistance to Minute virus of mice.
Mgat2 ablation in the myeloid lineage leads to defective glycoantigen T cell responses.
Infertility
MGAT1 and Complex N-Glycans Regulate ERK Signaling During Spermatogenesis.
Inflammatory Bowel Diseases
Promoter methylation of the MGAT3 and BACH2 genes correlates with the composition of the immunoglobulin G glycome in inflammatory bowel disease.
Insulin Resistance
Defective Phosphatidylglycerol Remodeling Causes Hepatopathy, Linking Mitochondrial Dysfunction to Hepatosteatosis.
Diabetes prevalence in NZO females depends on estrogen action on liver fat content.
Epigenetic programming at the Mogat1 locus may link neonatal overnutrition with long-term hepatic steatosis and insulin resistance.
Genetic variants near the MGAT1 gene are associated with body weight, BMI and fatty acid metabolism among adults and children.
Glycerolipid acyltransferases in triglyceride metabolism and energy homeostasis-potential as drug targets.
MGAT2 deficiency ameliorates high-fat diet-induced obesity and insulin resistance by inhibiting intestinal fat absorption in mice.
Multiple antisense oligonucleotides targeted against monoacylglycerol acyltransferase 1 (Mogat1) improve glucose metabolism independently of Mogat1.
Lipodystrophy
Mogat1 deletion does not ameliorate hepatic steatosis in lipodystrophic (Agpat2-/-) or obese (ob/ob) mice.
Liver Diseases
Monoacylglycerol O-acyltransferase 1 is regulated by peroxisome proliferator-activated receptor ? in human hepatocytes and increases lipid accumulation.
Regular moderate aerobic exercise improves high-fat diet-induced nonalcoholic fatty liver disease via monoacylglycerol O-acyltransferase 1 pathway suppression.
Suppression of PPAR?-mediated monoacylglycerol O-acyltransferase 1 expression ameliorates alcoholic hepatic steatosis.
Liver Neoplasms
Progression of hepatic neoplasms is severely retarded in mice lacking the bisecting N-acetylglucosamine on N-glycans: evidence for a glycoprotein factor that facilitates hepatic tumor progression.
Metabolic Diseases
Characterization of monoacylglycerol acyltransferase 2 inhibitors by a novel probe in binding assays.
Defective Phosphatidylglycerol Remodeling Causes Hepatopathy, Linking Mitochondrial Dysfunction to Hepatosteatosis.
Deficiency of the intestinal enzyme acyl CoA:monoacylglycerol acyltransferase-2 protects mice from metabolic disorders induced by high-fat feeding.
Discovery of a Novel Series of N-Phenylindoline-5-sulfonamide Derivatives as Potent, Selective, and Orally Bioavailable Acyl CoA:Monoacylglycerol Acyltransferase-2 Inhibitors.
Hepatic Monoacylglycerol O-acyltransferase 1 as a Promising Therapeutic Target for Steatosis, Obesity, and Type 2 Diabetes.
Inhibition of MGAT2 modulates fat-induced gut peptide release and fat intake in normal mice and ameliorates obesity and diabetes in ob/ob mice fed on a high-fat diet.
Monoacylglycerol Acyltransferase 2 (MGAT2) Inhibitors for the Treatment of Metabolic Diseases and Nonalcoholic Steatohepatitis (NASH).
Novel LC/MS/MS and High-Throughput Mass Spectrometric Assays for Monoacylglycerol Acyltransferase Inhibitors.
Metabolic Syndrome
Identification and design of a novel series of MGAT2 inhibitors.
MOGAT2: A New Therapeutic Target for Metabolic Syndrome.
Multiple Sclerosis
Family studies of type 1 diabetes reveal additive and epistatic effects between MGAT1 and three other polymorphisms.
Hypomorphic MGAT5 polymorphisms promote multiple sclerosis cooperatively with MGAT1 and interleukin-2 and 7 receptor variants.
Neoplasm Metastasis
Altered glycosylation associated with dedifferentiation of hepatocellular carcinoma: a lectin microarray-based study.
Bisected, complex N-glycans and galectins in mouse mammary tumor progression and human breast cancer.
Exosomal miR?663b exposed to TGF??1 promotes cervical cancer metastasis and epithelial?mesenchymal transition by targeting MGAT3.
MGAT3-mediated glycosylation of tetraspanin CD82 at asparagine 157 suppresses ovarian cancer metastasis by inhibiting the integrin signaling pathway.
Suppression of Cancer Progression by MGAT1 shRNA Knockdown.
The bisecting GlcNAc on N-glycans inhibits growth factor signaling and retards mammary tumor progression.
Neoplasms
Altered glycosylation associated with dedifferentiation of hepatocellular carcinoma: a lectin microarray-based study.
Bisected, complex N-glycans and galectins in mouse mammary tumor progression and human breast cancer.
Epigenetic activation of MGAT3 and corresponding bisecting GlcNAc shortens the survival of cancer patients.
Exosomal miR?663b exposed to TGF??1 promotes cervical cancer metastasis and epithelial?mesenchymal transition by targeting MGAT3.
Glyco-genes change expression in cancer through aberrant methylation.
Glycosylation regulates NK cell-mediated effector function through PI3K pathway.
Mevalonate Pathway Inhibition Slows Breast Cancer Metastasis via Reduced N-glycosylation Abundance and Branching.
MGAT1 is a novel transcriptional target of Wnt/?-catenin signaling pathway.
New evidence for an extra-hepatic role of N-acetylglucosaminyltransferase III in the progression of diethylnitrosamine-induced liver tumors in mice.
Novel DNA methylation sites associated with cigarette smoking among African Americans.
Progression of hepatic neoplasms is severely retarded in mice lacking the bisecting N-acetylglucosamine on N-glycans: evidence for a glycoprotein factor that facilitates hepatic tumor progression.
Reduced hepatocyte proliferation is the basis of retarded liver tumor progression and liver regeneration in mice lacking N-acetylglucosaminyltransferase III.
Reduced N-acetylglucosaminyltransferase III expression via Smad3 and Erk signaling in TGF-?1-induced HCC EMT model.
Suppression of Cancer Progression by MGAT1 shRNA Knockdown.
The bisecting GlcNAc in cell growth control and tumor progression.
The bisecting GlcNAc on N-glycans inhibits growth factor signaling and retards mammary tumor progression.
Truncated, inactive N-acetylglucosaminyltransferase III (GlcNAc-TIII) induces neurological and other traits absent in mice that lack GlcNAc-TIII.
Neuralgia
Novel mouse GABA uptake inhibitors with enhanced inhibitory activity toward mGAT3/4 and their effect on pain threshold in mice.
Neuroblastoma
Acquired genetic alterations in tumor cells dictate the development of high-risk neuroblastoma and clinical outcomes.
GABA transporter function, oligomerization state, and anchoring: correlates with subcellularly resolved FRET.
Lack of complex type N-glycans lessens aberrant neuronal properties.
Non-alcoholic Fatty Liver Disease
Characterization of the variability in the extent of nonalcoholic fatty liver induced by a high-fat diet in the genetically diverse Collaborative Cross mouse model.
Defective Phosphatidylglycerol Remodeling Causes Hepatopathy, Linking Mitochondrial Dysfunction to Hepatosteatosis.
Evidence for regulated monoacylglycerol acyltransferase expression and activity in human liver.
Inhibiting monoacylglycerol acyltransferase 1 ameliorates hepatic metabolic abnormalities but not inflammation and injury in mice.
Monoacylglycerol acyltransferase 1 knockdown exacerbates hepatic ischemia-reperfusion injury in mice with hepatic steatosis.
Monoacylglycerol Acyltransferase 2 (MGAT2) Inhibitors for the Treatment of Metabolic Diseases and Nonalcoholic Steatohepatitis (NASH).
Monoacylglycerol O-acyltransferase 1 is regulated by peroxisome proliferator-activated receptor ? in human hepatocytes and increases lipid accumulation.
Regular moderate aerobic exercise improves high-fat diet-induced nonalcoholic fatty liver disease via monoacylglycerol O-acyltransferase 1 pathway suppression.
Obesity
A predominant role of acyl-CoA:monoacylglycerol acyltransferase-2 in dietary fat absorption implicated by tissue distribution, subcellular localization, and up-regulation by high fat diet.
Adult-onset deficiency of acyl CoA:monoacylglycerol acyltransferase 2 protects mice from diet-induced obesity and glucose intolerance.
Cell-based assay of MGAT2-driven diacylglycerol synthesis for profiling inhibitors: use of a stable isotope-labeled substrate and high-resolution LC/MS.
Defective Phosphatidylglycerol Remodeling Causes Hepatopathy, Linking Mitochondrial Dysfunction to Hepatosteatosis.
Deficiency of MGAT2 increases energy expenditure without high-fat feeding and protects genetically obese mice from excessive weight gain.
Deficiency of the intestinal enzyme acyl CoA:monoacylglycerol acyltransferase-2 protects mice from metabolic disorders induced by high-fat feeding.
Discovery of a Novel Series of N-Phenylindoline-5-sulfonamide Derivatives as Potent, Selective, and Orally Bioavailable Acyl CoA:Monoacylglycerol Acyltransferase-2 Inhibitors.
Evidence for a Role of LPGAT1 in Influencing BMI and Percent Body Fat in Native Americans.
Evidence for a role of LPGAT1 in influencing BMI and percent body fat in native Americans.
Genetic variants near the MGAT1 gene are associated with body weight, BMI and fatty acid metabolism among adults and children.
Glycerolipid acyltransferases in triglyceride metabolism and energy homeostasis-potential as drug targets.
Hepatic Monoacylglycerol O-acyltransferase 1 as a Promising Therapeutic Target for Steatosis, Obesity, and Type 2 Diabetes.
Identification and design of a novel series of MGAT2 inhibitors.
Identification of 2-[2-(4-tert-butylphenyl)ethyl]-N-(4-fluorophenyl)-1,2,3,4-tetrahydroisoquinoline-6-sulfonamide (29) as an orally available MGAT2 inhibitor.
Inhibition of MGAT2 modulates fat-induced gut peptide release and fat intake in normal mice and ameliorates obesity and diabetes in ob/ob mice fed on a high-fat diet.
Intestine-specific deletion of acyl-CoA:monoacylglycerol acyltransferase (MGAT) 2 protects mice from diet-induced obesity and glucose intolerance.
Intestine-specific expression of MOGAT2 partially restores metabolic efficiency in Mogat2-deficient mice.
JTP-103237, a novel monoacylglycerol acyltransferase inhibitor, modulates fat absorption and prevents diet-induced obesity.
Many obesity-associated SNPs strongly associate with DNA methylation changes at proximal promoters and enhancers.
MGAT2 deficiency ameliorates high-fat diet-induced obesity and insulin resistance by inhibiting intestinal fat absorption in mice.
MGAT2 deficiency and vertical sleeve gastrectomy have independent metabolic effects in the mouse.
MGAT2, a monoacylglycerol acyltransferase expressed in the small intestine.
Mogat1 deletion does not ameliorate hepatic steatosis in lipodystrophic (Agpat2-/-) or obese (ob/ob) mice.
Multiple antisense oligonucleotides targeted against monoacylglycerol acyltransferase 1 (Mogat1) improve glucose metabolism independently of Mogat1.
Novel Cell-Based Assay to Investigate Monoacylglycerol Acyltransferase 2 Inhibitory Activity Using HIEC-6 Cell Line.
Nuclear receptor PPAR?-regulated monoacylglycerol O-acyltransferase 1 (MGAT1) expression is responsible for the lipid accumulation in diet-induced hepatic steatosis.
Optimization of a novel series of N-phenylindoline-5-sulfonamide-based acyl CoA:monoacylglycerol acyltransferase-2 inhibitors: Mitigation of CYP3A4 time-dependent inhibition and phototoxic liabilities.
Pharmacological characterization of a series of aryl-sulfonamide derivatives that potently and selectively inhibit monoacylglycerol acyltransferase 2.
Pharmacological Inhibition of Monoacylglycerol O-Acyltransferase 2 Improves Hyperlipidemia, Obesity, and Diabetes by Change in Intestinal Fat Utilization.
Properties of the mouse intestinal acyl-CoA:monoacylglycerol acyltransferase, MGAT2.
The rs4285184 polymorphism of the MGAT1 gene as a risk factor for obesity in the Mexican population.
Obesity, Morbid
Inhibition of MGAT2 modulates fat-induced gut peptide release and fat intake in normal mice and ameliorates obesity and diabetes in ob/ob mice fed on a high-fat diet.
Ovarian Neoplasms
Epigenetic activation of MGAT3 and corresponding bisecting GlcNAc shortens the survival of cancer patients.
In this issue: Proteomics 16/2008.
MGAT3-mediated glycosylation of tetraspanin CD82 at asparagine 157 suppresses ovarian cancer metastasis by inhibiting the integrin signaling pathway.
Specific glycosylation of membrane proteins in epithelial ovarian cancer cell lines: glycan structures reflect gene expression and DNA methylation status.
Overnutrition
Epigenetic programming at the Mogat1 locus may link neonatal overnutrition with long-term hepatic steatosis and insulin resistance.
Overweight
Hepatic Monoacylglycerol O-acyltransferase 1 as a Promising Therapeutic Target for Steatosis, Obesity, and Type 2 Diabetes.
Pancreatic Neoplasms
Associations between genetic variants of KIF5B, FMN1, and MGAT3 in the cadherin pathway and pancreatic cancer risk.
Prostatic Neoplasms
Suppression of Cancer Progression by MGAT1 shRNA Knockdown.
Starvation
N-acetylglucosaminyltransferase I promotes glioma cell proliferation and migration through increasing the stability of the glucose transporter GLUT1.
Uterine Cervical Neoplasms
Exosomal miR?663b exposed to TGF??1 promotes cervical cancer metastasis and epithelial?mesenchymal transition by targeting MGAT3.