EC Number |
General Information |
Reference |
---|
3.1.1.23 | evolution |
human monoacylglycerol lipase (MAGL) is a soluble serine hydrolase that belongs to the alpha/beta hydrolase fold superfamily |
749555 |
3.1.1.23 | evolution |
the enzyme is a member of the serine hydrolase superfamily |
751072 |
3.1.1.23 | evolution |
the GxSxS motif is conserved in monoacylglycerol lipases (MAGLs) |
749639 |
3.1.1.23 | malfunction |
amino acid changes of the GxSxG motif in AtMAGL6 alters the nucleophilic elbow structure, which is the active site of MAGLs. Mutating the GxSxG motif in the recombinant maltose binding protein (MBP):AtMAGL6 protein to SxSxG, GxAxG, and GxSxS motifs completely demolishes the activities of the mutant MAGL |
749639 |
3.1.1.23 | malfunction |
computational modeling shows that amino acid changes of the GxSxG motif in AtMAGL8 alters the nucleophilic elbow structure, which is the active site of MAGLs. Mutating the GxSxG motif in the recombinant maltose binding protein (MBP):AtMAGL8 protein to SxSxG, GxAxG, and GxSxS motifs completely demolishes the activities of the mutant MAGL |
749639 |
3.1.1.23 | malfunction |
deficiency of monoacylglycerol lipase (MGLL) results in lipid overload in tumor-associated macrophages. MGLL deficiency promotes CB2/TLR4-dependent macrophage activation, which further suppresses the function of tumor-associated CD8+ T cells, and contributes to lipid accumulation. Treatment with CB2 antagonists delays tumor progression in inoculated and genetic cancer models |
751669 |
3.1.1.23 | malfunction |
disruption of MAGL expression and activity impairs cancer pathogenicity. impairments in MAGL-dependent tumor growth are rescued by a high-fat diet, indicating that exogenous sources of fatty acids can contribute to malignancy in cancers lacking MAGL activity |
714693 |
3.1.1.23 | malfunction |
enzyme inactivation attenuates hepatic ischemia/reperfusion-induced tissue injury, inflammation and oxidative stress |
729792 |
3.1.1.23 | malfunction |
inhibition of monoacylglycerol lipase activity decreases glucose-stimulated insulin secretion in INS-1 (832/13) cells and rat islets |
-, 751941 |
3.1.1.23 | malfunction |
MGL inactivation drives a CB1 cannabinoid receptor-dependent axonal growth response |
715990 |