|
Congenital disorder of glycosylation type 2A
|
0.920 |
GeneticVariation
|
disease |
BEFREE |
However, crossing the Mgat2 mutation into a distinct genetic background resulted in a low frequency of survivors exhibiting additional and novel disease signs of CDG-IIa.
|
12417412 |
2002 |
|
Congenital disorder of glycosylation type 2A
|
0.920 |
GeneticVariation
|
disease |
BEFREE |
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.
|
8808595 |
1996 |
|
Obesity
|
0.040 |
AlteredExpression
|
disease |
BEFREE |
Pre-existing maternal obesity and GDM are associated with decreased expression in genes involved in fatty acid uptake and intracellular transport (LPL, FATP2, FATP6, FABPpm and ASCL1), triacylglyceride (TAG) biosynthesis (MGAT1,7 MGAT2 and DGAT1), lipogenesis (FASN) and lipolysis (PNPLA2, HSL and MGLL).
|
24262292 |
2014 |
|
Obesity
|
0.040 |
Biomarker
|
disease |
BEFREE |
Our results suggest that MGAT2 modulates energy expenditure through multiple mechanisms, including one independent of dietary fat; these findings also raise the prospect of inhibiting MGAT2 as a strategy for combating obesity and related metabolic disorders resulting from excessive calorie intake.
|
21734185 |
2011 |
|
Obesity
|
0.040 |
Biomarker
|
disease |
BEFREE |
The described cell-based assay adds a new methodology for the development and evaluation of MGAT2 inhibitors for the treatment of obesity and type 2 diabetes.
|
25598079 |
2015 |
|
Obesity
|
0.040 |
Biomarker
|
disease |
BEFREE |
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.
|
31837122 |
2020 |
|
Congenital Disorders of Glycosylation
|
0.040 |
GeneticVariation
|
group |
BEFREE |
The genes reported for CDG with NIHF for 15 distinct families include: PMM2 in 47% (7/15), ALG9 in 20% (3/15), ALG8 in 13% (2/15), ALG1 in 7% (1/15), MGAT2 in 7% (1/15), and COG6 7% (1/15).
|
31420886 |
2020 |
|
Congenital Disorders of Glycosylation
|
0.040 |
GeneticVariation
|
group |
BEFREE |
Based on molecular studies, the 27 CDG patients were classified into different subtypes: ALG9-CDG (8 patients, 29.5%), ALG3-CDG (7 patients, 26%), COG6-CDG (7 patients, 26%), MGAT2-CDG (3 patients, 11%), SLC35A2-CDG (1 patient), and PMM2-CDG (1 patient).
|
28742265 |
2017 |
|
Congenital Disorders of Glycosylation
|
0.040 |
GeneticVariation
|
group |
BEFREE |
Fibroblast extracts from two patients with a recently described variant of this disease (CDGS type II) have previously been shown to have over 98% reduced activity of UDP-GlcNAc:alpha-6-D-mannoside beta-1,2-N-acetylglucosaminyltransferase II [GlcNAc-TII; Jaeken, J., Schachter, H., Carchon, H., De Cock, P., Coddeville, B.& Spik, G. (1994) Arch.Dis.Childhood 71, 123-127].
|
7607254 |
1995 |
|
Congenital Disorders of Glycosylation
|
0.040 |
GeneticVariation
|
group |
BEFREE |
Two unrelated CDGS type II patients are shown to have point mutations (one patient having Ser-->Phe and the other having His-->Arg) in the catalytic domain of the gene MGAT2, encoding UDP-GlcNAc:alpha-6-D-mannoside beta-1,2-N- acetylglucosaminyltransferase II (GnT II), an enzyme essential for biosynthesis of complex Asn-linked glycans.
|
8808595 |
1996 |
|
Metabolic Diseases
|
0.030 |
Biomarker
|
group |
BEFREE |
MGAT1 and MGAT2 are both implicated in obesity-related metabolic diseases.
|
28328322 |
2017 |
|
Metabolic Diseases
|
0.030 |
Biomarker
|
group |
BEFREE |
Our results suggest that MGAT2 modulates energy expenditure through multiple mechanisms, including one independent of dietary fat; these findings also raise the prospect of inhibiting MGAT2 as a strategy for combating obesity and related metabolic disorders resulting from excessive calorie intake.
|
21734185 |
2011 |
|
Metabolic Diseases
|
0.030 |
Biomarker
|
group |
BEFREE |
This report first discusses the biological rationale in support of inhibition of MGAT2 as a therapeutic approach that may offer a distinct and superior efficacy versus GI tolerability profile and then reviews advances in the discovery of small molecule MGAT2 inhibitors for the treatment of metabolic diseases and nonalcoholic steatohepatitis (NASH).
|
29986142 |
2018 |
|
Diabetes
|
0.010 |
Biomarker
|
disease |
BEFREE |
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.
|
31837122 |
2020 |
|
Diabetes Mellitus
|
0.010 |
Biomarker
|
group |
BEFREE |
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.
|
31837122 |
2020 |
|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.010 |
Biomarker
|
disease |
BEFREE |
The described cell-based assay adds a new methodology for the development and evaluation of MGAT2 inhibitors for the treatment of obesity and type 2 diabetes.
|
25598079 |
2015 |
|
Neoplasms
|
0.010 |
Biomarker
|
group |
BEFREE |
To demonstrate monoacylglycerol acyltransferase 2 (MGAT2)-mediated enzyme activity in a cellular context, cells of the murine secretin tumor cell-1 line of enteroendocrine origin were used to construct human MGAT2-expressing recombinant cell lines.
|
25598079 |
2015 |
|
Neuroblastoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Further, the N-glycosylation pathway in the NB_1(-Mgat2) cell line was rescued by transiently transfecting cells with Mgat2, thus creating the NB_1(-/+Mgat2) cell line.
|
29902282 |
2018 |
|
Gestational Diabetes
|
0.010 |
AlteredExpression
|
phenotype |
BEFREE |
Pre-existing maternal obesity and GDM are associated with decreased expression in genes involved in fatty acid uptake and intracellular transport (LPL, FATP2, FATP6, FABPpm and ASCL1), triacylglyceride (TAG) biosynthesis (MGAT1,7 MGAT2 and DGAT1), lipogenesis (FASN) and lipolysis (PNPLA2, HSL and MGLL).
|
24262292 |
2014 |
|
Hydrops Fetalis, Non-Immune
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
The genes reported for CDG with NIHF for 15 distinct families include: PMM2 in 47% (7/15), ALG9 in 20% (3/15), ALG8 in 13% (2/15), ALG1 in 7% (1/15), MGAT2 in 7% (1/15), and COG6 7% (1/15).
|
31420886 |
2020 |
|
Central neuroblastoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Further, the N-glycosylation pathway in the NB_1(-Mgat2) cell line was rescued by transiently transfecting cells with Mgat2, thus creating the NB_1(-/+Mgat2) cell line.
|
29902282 |
2018 |
|
Congenital dyserythropoietic anemia, type II
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
Molecular cloning of the GnT II and alpha-Man II DNA sequences has allowed direct investigation of the genetic mutations underlying the glycosylation defect in CDA II patients to begin.
|
9009444 |
1997 |
|
GRANULOMATOUS DISEASE, CHRONIC, AUTOSOMAL RECESSIVE, CYTOCHROME b-POSITIVE, TYPE III
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
Based on molecular studies, the 27 CDG patients were classified into different subtypes: ALG9-CDG (8 patients, 29.5%), ALG3-CDG (7 patients, 26%), COG6-CDG (7 patients, 26%), MGAT2-CDG (3 patients, 11%), SLC35A2-CDG (1 patient), and PMM2-CDG (1 patient).
|
28742265 |
2017 |
|
Nonalcoholic Steatohepatitis
|
0.010 |
Biomarker
|
disease |
BEFREE |
This report first discusses the biological rationale in support of inhibition of MGAT2 as a therapeutic approach that may offer a distinct and superior efficacy versus GI tolerability profile and then reviews advances in the discovery of small molecule MGAT2 inhibitors for the treatment of metabolic diseases and nonalcoholic steatohepatitis (NASH).
|
29986142 |
2018 |
|
Childhood Neuroblastoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Further, the N-glycosylation pathway in the NB_1(-Mgat2) cell line was rescued by transiently transfecting cells with Mgat2, thus creating the NB_1(-/+Mgat2) cell line.
|
29902282 |
2018 |