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1,2-di-(9Z-octadecenoyl)-sn-glycerol + H2O
(9Z)-octadecenoate + 2-(9Z-octadecenoyl)-glycerol
the reaction proceeds in the forward direction
-
-
?
1-(9Z-octadecenoyl)-2-(5Z,8Z,11Z,14Z-eicosatetraenoyl)-sn-glycerol + H2O
(9Z)-octadecenoate + 2-(5Z,8Z,11Z,14Z-eicosatetraenoyl)-glycerol
the reaction proceeds in the forward direction
-
-
?
1-(9Z-octadecenoyl)-2-(9Z,12Z-octadecadienoyl)-sn-glycerol + H2O
(9Z)-octadecenoate + 2-(9Z,12Z-octadecadienoyl)-glycerol
the reaction proceeds in the forward direction
-
-
?
1-(9Z-octadecenoyl)-2-O-(5Z,8Z,11Z,14Z-eicosatetraenoyl)-sn-glycerol + H2O
(9Z)-octadecenoate + 2-O-(5Z,8Z,11Z,14Z)-eicosatetraenoylglycerol
the reaction proceeds in the forward direction
-
-
?
1-(9Z-octadecenoyl)-2-octadecanoyl-sn-glycerol + H2O
(9Z)-octadecenoate + 2-octadecanoylglycerol
the reaction proceeds in the forward direction
-
-
?
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
1-octadecanoyl-2-(5Z,8Z,11Z,14Z-eicosatetraenoyl)-sn-glycerol + H2O
2-(5Z,8Z,11Z,14Z-eicosatetraenoyl)-glycerol + octadecanoate
1-oleoyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + oleate
-
-
-
?
1-stearyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + stearate
-
preferred substrate, release of arachidonate from 2-arachidonyl diglyceride
-
-
?
1-stearyl-2-oleoyl-sn-glycerol + H2O
2-oleoylglycerol + stearate
-
-
-
-
?
sn-1-stearoyl-2-arachidonoyl-glycerol + H2O
2-arachidonoylglycerol + stearate
-
-
-
?
additional information
?
-
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
-
-
-
-
?
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
-
-
-
?
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
-
-
-
?
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
-
-
-
-
?
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
-
-
-
?
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
-
-
-
r
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
-
-
-
?
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
-
-
-
?
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
-
-
-
?
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
-
-
-
?
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
-
-
-
?
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
-
-
-
r
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
-
-
-
r
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
-
-
-
?
1-octadecanoyl-2-(5Z,8Z,11Z,14Z-eicosatetraenoyl)-sn-glycerol + H2O
2-(5Z,8Z,11Z,14Z-eicosatetraenoyl)-glycerol + octadecanoate
the reaction proceeds in the forward direction
-
-
?
1-octadecanoyl-2-(5Z,8Z,11Z,14Z-eicosatetraenoyl)-sn-glycerol + H2O
2-(5Z,8Z,11Z,14Z-eicosatetraenoyl)-glycerol + octadecanoate
the reaction proceeds in the forward reaction
-
-
?
additional information
?
-
assay optimization of DAGLbeta EnzChek assay using the using the purified catalytic domain (GST-DAGLbeta CD), overview
-
-
-
additional information
?
-
-
the diglyceride lipase utilizes 2-arachidonyl diglycerides as the best substrate. Positional specificity of the enzyme, no formation of 1-stearylglycerol, direct deacylation of diglyceride at sn-2 position does not occur. DG lipase exhibits the following order of substrate specificity in descending order: arachidonyl DG > eicosatrienoyl DG > linoleoyl DG = oleoyl DG
-
-
-
additional information
?
-
establishment of a DAGL activity assay based on competitive ABPP methods using a fluorophosphonate-rhodamine (FP-Rh) probe, labeling is blocked by the non-specific lipase inhibitor tetrahydrolipstatin in a dose-dependent manner. Opening the piperidyl ring of DAGLbeta inhibitors facilitates attachment of a BODIPY fluorophore to yield probe HT-01, which labels both DAGLbeta and DAGLalpha. HT-01 is about 5fold more active against DAGLbeta than FP-Rh
-
-
-
additional information
?
-
usage of a highly sensitive radiometric assay to measure DAGL activity by using 1-oleoyl[1-14C]-2-arachidonoylglycerol as the substrate. Isozymes DAGLalpha and DAGLbeta possess a catalytic triad typical of serine hydrolases, and do not exhibit strong selectivity for 2-arachidonate-containing DAG. 1-Oleoyl-2-arachidonoyl-sn-glycerol is obtained from the R(-)solketal esterified with oleic acid, using N'-(3-dimethylaminopropyl)-N-ethylcarbodiimide hydrochloride/4-dimethylaminopyridine, and deprotecting the acetonide with hydrochloride/methanol. The primary alcoholic group is selectively protected with triisopropylsilyl chloride, whereas the free secondary alcohol is esterified with arachidonic acid (AA). Finally, the 1-oleoyl-2-arachidonoylglycerol is obtained by selectively removing the sylyl group with tetrabutylammonium fluoride/acetic acid. Assay method, overview
-
-
-
additional information
?
-
usage of a highly sensitive radiometric assay to measure DAGL activity by using 1-oleoyl[1-14C]-2-arachidonoylglycerol as the substrate. Isozymes DAGLalpha and DAGLbeta possess a catalytic triad typical of serine hydrolases, and do not exhibit strong selectivity for 2-arachidonate-containing DAG. 1-Oleoyl-2-arachidonoyl-sn-glycerol is obtained from the R(-)solketal esterified with oleic acid, using N'-(3-dimethylaminopropyl)-N-ethylcarbodiimide hydrochloride/4-dimethylaminopyridine, and deprotecting the acetonide with hydrochloride/methanol. The primary alcoholic group is selectively protected with triisopropylsilyl chloride, whereas the free secondary alcohol is esterified with arachidonic acid (AA). Finally, the 1-oleoyl-2-arachidonoylglycerol is obtained by selectively removing the sylyl group with tetrabutylammonium fluoride/acetic acid. Assay method, overview
-
-
-
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1,2-di-(9Z-octadecenoyl)-sn-glycerol + H2O
(9Z)-octadecenoate + 2-(9Z-octadecenoyl)-glycerol
the reaction proceeds in the forward direction
-
-
?
1-(9Z-octadecenoyl)-2-(5Z,8Z,11Z,14Z-eicosatetraenoyl)-sn-glycerol + H2O
(9Z)-octadecenoate + 2-(5Z,8Z,11Z,14Z-eicosatetraenoyl)-glycerol
the reaction proceeds in the forward direction
-
-
?
1-(9Z-octadecenoyl)-2-(9Z,12Z-octadecadienoyl)-sn-glycerol + H2O
(9Z)-octadecenoate + 2-(9Z,12Z-octadecadienoyl)-glycerol
the reaction proceeds in the forward direction
-
-
?
1-(9Z-octadecenoyl)-2-O-(5Z,8Z,11Z,14Z-eicosatetraenoyl)-sn-glycerol + H2O
(9Z)-octadecenoate + 2-O-(5Z,8Z,11Z,14Z)-eicosatetraenoylglycerol
the reaction proceeds in the forward direction
-
-
?
1-(9Z-octadecenoyl)-2-octadecanoyl-sn-glycerol + H2O
(9Z)-octadecenoate + 2-octadecanoylglycerol
the reaction proceeds in the forward direction
-
-
?
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
1-octadecanoyl-2-(5Z,8Z,11Z,14Z-eicosatetraenoyl)-sn-glycerol + H2O
2-(5Z,8Z,11Z,14Z-eicosatetraenoyl)-glycerol + octadecanoate
1-oleoyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + oleate
-
-
-
?
sn-1-stearoyl-2-arachidonoyl-glycerol + H2O
2-arachidonoylglycerol + stearate
-
-
-
?
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
-
-
-
-
?
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
-
-
-
?
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
-
-
-
?
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
-
-
-
-
?
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
-
-
-
?
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
-
-
-
r
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
-
-
-
?
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
-
-
-
?
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
-
-
-
?
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
-
-
-
?
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
-
-
-
?
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
-
-
-
r
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
-
-
-
r
1-acyl-2-arachidonoyl-sn-glycerol + H2O
2-arachidonoylglycerol + fatty acid
-
-
-
?
1-octadecanoyl-2-(5Z,8Z,11Z,14Z-eicosatetraenoyl)-sn-glycerol + H2O
2-(5Z,8Z,11Z,14Z-eicosatetraenoyl)-glycerol + octadecanoate
the reaction proceeds in the forward direction
-
-
?
1-octadecanoyl-2-(5Z,8Z,11Z,14Z-eicosatetraenoyl)-sn-glycerol + H2O
2-(5Z,8Z,11Z,14Z-eicosatetraenoyl)-glycerol + octadecanoate
the reaction proceeds in the forward reaction
-
-
?
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((2R,5R)-2-benzyl-5-[(prop-2-yn-1-yl)oxy]piperidin-1-yl)(4-[bis(4-fluorophenyl)(hydroxy)methyl]-2H-1,2,3-triazol-2-yl)methanone
i.e. DH376, a covalent irreversible inhibitor that features a 2-benzylpiperidine moiety which confers selectivity and activity towards DAGLs and ABHD6
-
(2-benzylpiperidin-1-yl)[4-(2'-methoxy[1,1'-biphenyl]-4-yl)-1H-1,2,3-triazol-1-yl]methanone
-
-
(2-benzylpiperidin-1-yl)[4-([1,1'-biphenyl]-4-yl)-1H-1,2,3-triazol-1-yl]methanone
-
-
(4,4-difluoro-5,7-dimethyl-4-bora-3a,4a-diaza-s-indacine-3-yl)-N-(2-phenylethyl)-N-(5-propanamidopentyl)-4-[4-(trifluoromethoxy)phenyl]-1H-1,2,3-triazole-1-carboxamide
probe HT-01 labels both DAGLbeta and DAGLalpha. HT-01 is about 5fold more active against DAGLbeta than FP-Rh
-
(4-([1,1'-biphenyl]-4-yl)-1H-1,2,3-triazol-1-yl)((2R,3R)-2-((benzyloxy)methyl)-3-hydroxy-3,6-dihydropyridin-1(2H)-yl)methanone
-
-
(4-([1,1'-biphenyl]-4-yl)-1H-1,2,3-triazol-1-yl)((2S,3R)-2-((benzyloxy)methyl)-3-hydroxy-3,6-dihydropyridin-1(2H)-yl)methanone
-
-
(4-([1,1'-biphenyl]-4-yl)-1H-1,2,3-triazol-1-yl)((3R,6R)-6-((benzyloxy)methyl)-3-hydroxy-3,6-dihydropyridin-1(2H)-yl)methanone
-
-
(4-([1,1'-biphenyl]-4-yl)-1H-1,2,3-triazol-1-yl)((3R,6S)-6-((benzyloxy)methyl)-3-hydroxy-3,6-dihydropyridin-1(2H)-yl)methanone
-
-
(4-([1,1'-biphenyl]-4-yl)-1H-1,2,3-triazol-1-yl)((3R,6S)-6-benzyl-3-hydroxy-3,6-dihydropyridin-1(2H)-yl)methanone
-
-
(4-([1,1'-biphenyl]-4-yl)-1H-1,2,3-triazol-1-yl)((3S,6R)-6-((benzyloxy)methyl)-3-hydroxy-3,6-dihydropyridin-1(2H)-yl)methanone
-
-
(R)-(3-([1,1'-biphenyl]-4-yl)-1H-1,2,4-triazol-1-yl)(6-((benzyloxy)methyl)-3,6-dihydropyridin-1(2H)-yl)methanone
-
-
(R)-(3-([1,1'-biphenyl]-4-yl)-1H-pyrazol-1-yl)(6-((benzyloxy)methyl)-3,6-dihydropyridin-1(2H)-yl)methanone
-
-
(R)-(4-([1,1'-biphenyl]-4-yl)-1H-1,2,3-triazol-1-yl)(2-((benzyloxy)methyl)piperidin-1-yl)methanone
-
-
(R)-(4-([1,1'-biphenyl]-4-yl)-1H-1,2,3-triazol-1-yl)(6-((benzyloxy)methyl)-3,6-dihydropyridin-1(2H)-yl)methanone
-
-
(R)-(4-([1,1'-biphenyl]-4-yl)-1H-1,2,3-triazol-1-yl)(6-benzyl-3,6-dihydropyridin51(2H)-yl)methanone
-
-
(R)-(6-((benzyloxy)methyl)-3,6-dihydropyridin-1(2H)-yl)(3-(4-bromophenyl)-1H-pyrazol-1-yl)methanone
-
-
(R)-(6-((benzyloxy)methyl)-3,6-dihydropyridin-1(2H)-yl)(4-(4-bromophenyl)-1H-1,2,3-triazol-1-yl)methanone
-
-
(R)-(6-((benzyloxy)methyl)-3,6-dihydropyridin-1(2H)-yl)(4-(4-bromophenyl)-1H-imidazol-1-yl)methanone
-
-
(R)-(6-((benzyloxy)methyl)-3,6-dihydropyridin-1(2H)-yl)(4-(4-nitrophenyl)-1H-1,2,3-triazol-1-yl)methanone
-
-
(R)-(6-((benzyloxy)methyl)-3,6-dihydropyridin-1(2H)-yl)(4-(4-phenoxyphenyl)-1H-1,2,3-triazol-1-yl)methanone
-
-
(R)-(6-((benzyloxy)methyl)-3,6-dihydropyridin-1(2H)-yl)(4-phenyl-1H-1,2,3-triazol-1-yl)methanone
-
-
(S)-(4-([1,1'-biphenyl]-4-yl)-1H-1,2,3-triazol-1-yl)(6-((benzyloxy)methyl)-3,6-dihydropyridin-1(2H)-yl)methanone
-
-
4-hydroxymercuribenzoate
-
inhibits DG lipase 40% at 0.1 mM, while the MG lipase is completely inhibited
4-nitrophenyl (R)-6-((benzyloxy)methyl)-3,6-dihydropyridine-1(2H)-carboxylate
-
-
fluorophosphonate-rhodamine
FP-Rh, in this probe the fluorophosphonate is the reactive group (RG) as it binds irreversibly to the active-site serine nucleophile of serine hydrolases and the tag is rhodamine, a fluorophore for in-gel visualization
-
indomethacin
-
induces accumulation of DG in activated platelets by inhibiting DG lipase
p-hydroxy-mercuri-benzoate
-
RHC 80267
i.e. O,O'-[1,6-hexanediylbis(iminocarbonyl)]dioxime cyclohexanone or U 57908; i.e. O,O'-[1,6-hexanediylbis(iminocarbonyl)]dioxime cyclohexanone or U 57908
tert-butyl 3-benzyl-4-[4-[4-(trifluoromethoxy)phenyl]-1H-1,2,3-triazole-1-carbonyl]piperazine-1-carboxylate
-
-
tert-butyl 3-benzyl-4-{4-[4-(trifluoromethoxy)phenyl]-1H-1,2,3-triazole-1-carbonyl}piperazine-1-carboxylate
i.e. DO34, a covalent irreversible inhibitor that features a 2-benzylpiperidine moiety which confers selectivity and activity towards DAGLs and ABHD6
-
[(2R)-2-benzylpiperidin-1-yl][4-([1,1'-biphenyl]-4-yl)-1H-1,2,3-triazol-1-yl]methanone
-
-
[(2S)-2-benzylpiperidin-1-yl][4-([1,1'-biphenyl]-4-yl)-1H-1,2,3-triazol-1-yl]methanone
-
-
[(6S)-6-benzyl-3,6-dihydropyridin-1(2H)-yl][4-([1,1'-biphenyl]-4-yl)-1H-1,2,3-triazol-1-yl]methanone
-
-
[4-(4'-methoxy[1,1'-biphenyl]-4-yl)-1H-1,2,3-triazol-1-yl](2-phenylpiperidin-1-yl)methanone
-
-
[[(3R,6R)-6-benzyl-1-[4-[bis(4-fluorophenyl)(hydroxy)methyl]-2H-1,2,3-triazole-2-carbonyl]piperidin-3-yl]oxy]acetonitrile
-
-
RHC80267
blocks 2-AG formation from intact cells; blocks 2-AG formation from intact cells
RHC80267
a non-selective serine hydrolase inhibitor
tetrahydrolipstatin
THL
tetrahydrolipstatin
THL, THL inhibits the neurite outgrowth response stimulated by FGF2, at 100 nM it inhibits 66.7%, 93.5% and 99.2% of AG-2 release in N18-TG2, C6, and RBL-2H3 cells, respectively. IC50 of 0.002 mM for the inhibition by THL of FGF2 response; THL, THL inhibits the neurite outgrowth response stimulated by FGF2, at 100 nM it inhibits 66.7%, 93.5% and 99.2% of AG-2 release in N18-TG2, C6, and RBL-2H3 cells, respectively. IC50 of 0.002 mM for the inhibition by THL of FGF2 response
tetrahydrolipstatin
THL; THL
tetrahydrolipstatin
a non-selective serine hydrolase inhibitor, non-specific lipase inhibitor
additional information
-
the enzyme is sensitive to sulfhydryl inhibitors. MG lipase is much more sensitive to sulfhydryl inhibitors than DG lipase
-
additional information
high-throughput screening for DAGLbeta enzyme-specific inhibitors, assay optimization of DAGLbeta EnzChek assay using the using the purified catalytic domain (GST-DAGLbeta CD), overview
-
additional information
no inhibition by PMSF; no inhibition by PMSF
-
additional information
no inhibition by PMSF; no inhibition by PMSF
-
additional information
most DAGL inhibitors cross-react with alpha,beta-hydrolase domain containing protein 6 (ABHD6), which has a minor role in the hydrolysis of 2-AG, degrades bis-(monoacylglycero)-phosphate, and acts as a lysophosphatidyl hydrolase. Enantioselective synthesis and structure activity relationships of triazole ureas featuring chiral, hydroxylated 2-benzylpiperidines as dual inhibitors of DAGLalpha and ABHD6. The chirality of the carbon bearing the C2 substituent, as well as the position of the hydroxyl (tolerated at C5, but not at C3) has profound influence on the inhibitory activity of both DAGLalpha and ABHD6, as established using biochemical assays and competitive activity-based protein profiling on mouse brain extracts. pIC50 values. Structure-activity relationship of the covalent irreversible inhibitors, overview
-
additional information
a series of in vivo-active 1,2,3-triazole urea inhibitors, along with paired negative-control and activity-based probes, are used for the functional analysis of DAGLbeta in living systems. Optimized inhibitors show excellent selectivity for DAGLbeta over other serine hydrolases, including DAGLalpha (about 60fold selectivity), and the limited off-targets, such as ABHD6, are also inhibited by the negative-control probe. Establishment of a DAGL activity assay based on competitive ABPP methods using a fluorophosphonate-rhodamine (FP-Rh) probe, labeling is blocked by the non-specific lipase inhibitor tetrahydrolipstatin in a dose-dependent manner. Opening the piperidyl ring of DAGLbeta inhibitors facilitates attachment of a BODIPY fluorophore to yield probe HT-01, which labels both DAGLbeta and DAGLalpha. HT-01 is about 5fold more active against DAGLbeta than FP-Rh. In situ treatment of Neuro2A cells and peritoneal macrophages with inhibitors, overview
-
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additional information
the human DAGLbeta catalytic domain sequence corresponds to amino acids 228-672
malfunction
cholinergic innervation of CA1 pyramidal cells of the hippocampus is sensitive to the genetic disruption of 2-arachidonoylglycerol (2-AG) signaling in DAGLalpha null mice. Heterologous DAGLalpha overexpression spherically excludes cholinergic growth cones from 2-AG-rich extracellular environments, and minimizes cell-cell contact in vitro. Extracellular 2-AG concentrations can be sufficient to activate CB1Rs along discrete spherical boundaries to modulate neuronal responsiveness. The cholinergic phenotype brought about by DAGLalpha deletion exceeds that in DAGLbeta-/- mice, in which alterations to cholinergic synapse distribution are milder and more stochastic, precluding statistical significance. The overall density and average size of ChAT1 boutons remains unchanged
malfunction
DAGLalpha expression is dramatically downregulated when neural stem (NS) cells are differentiated toward a gamma-aminobutyric acidergic neuronal phenotype. Specific mutation within the GCbox that inhibits Sp1 binding reduced DAGLalpha promoter activity in NS cells. A dominant negative Sp1 is shown to bind to the GC-box and to suppress DAGLalpha promoter activity specifically in NS cells. Like DAGLalpha, Sp1 is downregulated during neuronal differentiation
malfunction
DAGLbeta inhibition perturbs a lipid network involved in macrophage inflammatory responses. DAGLbeta inactivation lowers 2-arachidonoylglycerol (2-AG) content, as well as arachidonic acid and eicosanoids contents, in mouse peritoneal macrophages in a manner that is distinct and complementary to disruption of cytosolic phospholipase-A2 (PLA2G4A). A corresponding reduction in lipopolysaccharide-induced tumor necrosis factor-alpha release is observed
malfunction
knockdown models in OSCC-derived cell lines for DAGLA (siDAGLA) and treatment with a lipase inhibitor (orlistat) show several depressed cellular functions, including cellular proliferation and migratory activities through cell-cycle arrest at G1 phase
malfunction
pharmacological elimination of 2-arachidonoylglycerol (2-AG) hydrolytic activity in rat brain sections leads to an accumulation of endogenous 2-AG and subsequent CB1 receptor activation. The brain regional CB1 receptor-Gi/o-activity largely remains unaltered in DAGLalpha-knockout and DAGLbeta-knockout mice when compared to wild-type littermates. Following comprehensive pharmacological blockade of 2-AG hydrolysis, brain sections generate sufficient amounts of 2-AG to activate CB1 receptors throughout the regions endowed with these receptors. As demonstrated by LC/MS/MS, this pool of 2-AG is generated via tetrahydrolipstatin-sensitive enzymatic pathways distinct from DAGLalpha or DAGLbeta. The DAGL activity generates 2-AG in sufficient amounts to activate CB1 receptors. The 2-AG accumulation is susceptible to two recognized inhibitors of the DAGLs, tetrahydrolipstatin (THL) and compound RHC80267 and CB1 receptor activity is modestly amplified by two DAGL activators, calcium and glutathione
malfunction
possible association between alcoholism and single nucleotide polymorphisms (SNPs) of the human DAGLA gene in Japanese population
metabolism
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DG lipase utilizes arachidonyl diglyceride as a preferred substrate and deacylates at sn-1 position with a pH optimum of 3.5, followed by MG lipase which hydrolyzes at sn-2 position with an alkaline pH optimum
metabolism
the diacylglycerol lipases (DAGLalpha and DAGLbeta) hydrolyze DAG to generate 2-arachidonoylglycerol (2-AG), the principal endocannabinoid and main precursor of arachidonic acid (AA). The DAGLs make distinct tissue specific contributions toward 2-AG and AA levels, and therefore, selective modulators for these enzymes could play crucial roles toward harnessing their therapeutic potential. DAGLbeta is a target for inflammatory diseases via mechanisms independent of the cannabinoid receptors whereas DAGLalpha is responsible for 2-AG mediated CB1 signaling at the synapse, and therefore, nonselectively targeting DAGLbeta (over DAGLalpha) could risk disrupting CB1 signaling at the synapse
metabolism
the primary pathway for 2-arachidonoylglycerol (2-AG) generation is believed to be conversion from the diacylglycerols (DAGs) by two sn-1-specific lipases, DAGLalpha and DAGLbeta
physiological function
diacylglycerol lipase alpha (DAGLA), which catalyzes the hydrolysis of diacylglycerol to 2-arachidonoylglycerol and free fatty acid, is required for axonal growth during the brain development and for retrograde synaptic signaling at mature synapses. Diacylglycerol lipase alpha promotes tumorigenesis in oral cancer by cell-cycle progression. DAGLA-positive oral squamous cell carcinomas (OSCCs) samples are correlated highly with the primary tumoral size. DAGLA may be a key determinant in tumoral progression and might be a therapeutic target for OSCCs
physiological function
endocannabinoids are small signaling lipids, with 2-arachidonoylglycerol (2-AG) implicated in modulating axonal growth and synaptic plasticity, concept of short-range extracellular signaling by endocannabinoids. Endocannabinoids, particularly 2-arachidonoylglycerol (2-AG) and anandamide (AEA), modulate synaptic neurotransmission by acting on molecularly diverse cannabinoid receptors in the brain. 2-AG is chiefly recognized as the retrograde messenger engaging presynaptic CB1 cannabinoid receptors (CB1Rs) to scale neurotransmitter release. Focusing on 2-AG signaling, the molecular architecture of endocannabinoid signaling during neurodevelopment is profoundly different from that in adult brain. Primary reliance of nervous system organization and function on DAGLalpha, 2-AG signaling is required for the spatial organization, rather than synaptogenesis per se, of cholinergic hippocampal projections. CB1Rs modulate GC motility and directional growth around DAGLalpha hot spots in vitro
physiological function
endocannabinoids are the endogenous ligands of the G protein-coupled cannabinoid receptors. The principal brain endocannabinoid, 2-arachidonoylglycerol (2-AG), is enzymatically produced from the diacylglycerols (DAGs) by two sn-1-specific lipases, DAGLalpha and DAGLbeta, in postsynaptic neurons and then activates presynaptic CB1 receptors in a retrograde manner. DAGLalpha is the major enzyme needed for retrograde synaptic 2-AG signalling. In addition to the sn-1-specific DAGLs, additional 2-AG generating enzymatic pathways are active in brain sections
physiological function
enzyme sn1-DAG lipase is involved in the spatial and temporal regulation of endocannabinoid signaling in the brain. The diacylglycerol (DAG) lipase activity is required for axonal growth during development and for retrograde synaptic signaling at mature synapses. This enzyme synthesizes the endocannabinoid 2-arachidonoyl-glycerol (2-AG), and the CB1 cannabinoid receptor is also required for the above responses
physiological function
isozyme DAGLbeta hydrolyzes diacylglycerol (DAG) to generate 2-arachidonoylglycerol (2-AG), the principal endocannabinoid and main precursor of arachidonic acid (AA)
physiological function
the diacylglycerol lipases (DAGLalpha and DAGLbeta) synthesize 2-arachidonoylglycerol (2-AG), a full agonist at cannabinoid receptors. Dynamic regulation of DAGL expression underpins its role in axonal growth and guidance during development, retrograde synaptic signalling at mature synapses, and maintenance of adult neurogenesis. DAGLalpha is expressed in a number of NS cell lines, where it drives cell proliferation via activation of both CB1 and CB2 receptors
physiological function
the endocannabinoid 2-arachidonoylglycerol (2-AG) exerts its physiological action by binding to and functionally activating type-1 (CB1) and type-2 (CB2) cannabinoid receptors. It is produced through the action of sn-1 selective diacylglycerol lipase (DAGL) that catalyzes 2-AG biosynthesis from sn-2-arachidonate-containing diacylglycerols
physiological function
the endocannabinoid 2-arachidonoylglycerol (2-AG) is biosynthesized by diacylglycerol lipases DAGLalpha and DAGLbeta. DAGLbeta is a key metabolic hub within a lipid network that regulates proinflammatory responses in macrophages. Using a combination of inhibitors and knockout mice, strong evidence is generated that both DAGLbeta and PLA2G4A contribute to prostaglandin production in lipopolysaccharide-stimulated macrophages
physiological function
the endocannabinoid system is involved in neuropsychiatric diseases, in addiction and other mental disorders including depression, posttraumatic stress disorder and schizophrenia. The endocannabinoid system regulates as a filter of input signal to dopaminergic neuron with dramatic changes in the reward-relevant brain, such as in the midbrain and in the stratum during alcohol intake, alcohol deprivation, and relapse. 2-Arachidonoyl glycerol (2-AG) is one of the two main endocannabinoids, and their regulation can play roles in the disorders under the environmental influence. Involvement of diacylglycerol lipase alpha (DAGLA), that is a 2-AG biosynthesizing enzyme in the pathogenesis of alcoholism, and possible association between alcoholism and single nucleotide polymorphisms (SNPs) of the human DAGLA gene in Japanese population. The involvement of DAGLA in alcoholism is possible by its genetic dysfunction and also by influence of stress. Analysis of interaction of DAGLA gene and stress, overview
physiological function
the endocannabinoid system is involved in neuropsychiatric diseases, in addiction and other mental disorders including depression, posttraumatic stress disorder and schizophrenia. The endocannabinoid system regulates as a filter of input signal to dopaminergic neuron with dramatic changes in the reward-relevant brain, such as in the midbrain and in the stratum during alcohol intake, alcohol deprivation, and relapse. Analysis of interaction of DAGLA gene and stress, overview. Considerable correlation is observed between alcohol preference and the Dagla expression. More preference to alcohol seems to induce more reduction of the Dagla expression in the brain of mice, while the mice intraperitoneally injected with 4% alcohol for 7 days show no difference from the mice injected with saline indicating that the difference of Dagla gene is not due to the amount of ethanol consumption in mice
physiological function
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the sequential action of a PI-specific phospholipase C and a diacylglyceride lipase (DG lipase) may serve as a potential means of releasing arachidonate in intact platelets. DG lipase may play an important role in releasing arachidonate
physiological function
-
the endocannabinoid system is involved in neuropsychiatric diseases, in addiction and other mental disorders including depression, posttraumatic stress disorder and schizophrenia. The endocannabinoid system regulates as a filter of input signal to dopaminergic neuron with dramatic changes in the reward-relevant brain, such as in the midbrain and in the stratum during alcohol intake, alcohol deprivation, and relapse. Analysis of interaction of DAGLA gene and stress, overview. Considerable correlation is observed between alcohol preference and the Dagla expression. More preference to alcohol seems to induce more reduction of the Dagla expression in the brain of mice, while the mice intraperitoneally injected with 4% alcohol for 7 days show no difference from the mice injected with saline indicating that the difference of Dagla gene is not due to the amount of ethanol consumption in mice
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additional information
a dominant negative Sp1 is shown to bind to the GC-box and to suppress DAGLalpha promoter activity specifically in NS cells
additional information
generation and cell-cycle analysis of enzyme deficient siDAGLA cells. Overexpression of DAGLA controls cellular proliferation in OSCC cells and clinical samples through cell-cycle progression. DAGLA-positive OSCC is correlated highly with the primary tumoral size. OSCC cells (KOSC-2 and Ho-1-N-1) are injected subcutaneously into the backs of female nude mice. The tumoral volume of the orlistat-treated group is clearly smaller than that of the control group. DAGLA inhibitor orlistat does not affect the body weight of the mice compared with the control group
additional information
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generation and cell-cycle analysis of enzyme deficient siDAGLA cells. Overexpression of DAGLA controls cellular proliferation in OSCC cells and clinical samples through cell-cycle progression. DAGLA-positive OSCC is correlated highly with the primary tumoral size. OSCC cells (KOSC-2 and Ho-1-N-1) are injected subcutaneously into the backs of female nude mice. The tumoral volume of the orlistat-treated group is clearly smaller than that of the control group. DAGLA inhibitor orlistat does not affect the body weight of the mice compared with the control group
additional information
genotyping, three SNPs in the DAGLA gene, rs879486(C_8906779_10), rs9735635(C_25958391_10) and rs3741252/Pro899Leu(C_25959741_10), are used for screening as tag SNPs across the gene. One of those SNPs, rs879486, is excluded from the final analysis in all the subjects, since rs879486 does not show association with alcoholism in the Japanese subjects. But associations are observed for the other two polymorphisms, rs9735635 and rs3741252/Pro899Leu, in the screening. Significant differences are found between those two polymorphisms and alcoholism in the Japanese population studied
additional information
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genotyping, three SNPs in the DAGLA gene, rs879486(C_8906779_10), rs9735635(C_25958391_10) and rs3741252/Pro899Leu(C_25959741_10), are used for screening as tag SNPs across the gene. One of those SNPs, rs879486, is excluded from the final analysis in all the subjects, since rs879486 does not show association with alcoholism in the Japanese subjects. But associations are observed for the other two polymorphisms, rs9735635 and rs3741252/Pro899Leu, in the screening. Significant differences are found between those two polymorphisms and alcoholism in the Japanese population studied
additional information
brain regional CB1 receptor-Gi/o-activity largely remains unaltered in DAGLalpha-knockout and DAGLb-knockout mice when compared to wild-type littermates. Following comprehensive pharmacological blockade of 2-AG hydrolysis, brain sections generate sufficient amounts of 2-AG to activate CB1 receptors throughout the regions endowed with these receptors. As demonstrated by LC/MS/MS, this pool of 2-AG is generated via tetrahydrolipstatin-sensitive enzymatic pathways distinct from DAGLalpha or DAGLbeta. Blockade of endocannabinoid hydrolysis by the irreversibly acting inhibitor MAFP evokes CP55,940-mimicking [35S]GTPgammaS binding responses throughout the CB1 receptor enriched brain regions of DAGLalpha-KO, DAGLbeta-KO, and WT mice brain sections. No statistically significant difference is observed in CP55,940-evoked regional CB1 receptor activity between DAGLb-KO and wild-type mice whereas in certain hippocampal regions of DAGLalpha-KO mice (hippocampus-overall, hippocampus-CA3 and hippocampus-dentate gyrus), sub-maximal concentrations of CP55,940 evoke a statistically significant increase in CB1 receptor activity. The observed labelling patterns evoked by both MAFP and CP55,940 are abolished with the CB1 receptor-selective antagonist AM251, confirming that responses are being mediated via the CB1 receptors. Comparison of 2-AG and anandamide (AEA, the other principal endocannabinoid) levels between unprocessed cryosections of DAGLalpha-KO, DAGLbeta-KO and wild-type mice brains
additional information
brain regional CB1 receptor-Gi/o-activity largely remains unaltered in DAGLalpha-knockout and DAGLb-knockout mice when compared to wild-type littermates. Following comprehensive pharmacological blockade of 2-AG hydrolysis, brain sections generate sufficient amounts of 2-AG to activate CB1 receptors throughout the regions endowed with these receptors. As demonstrated by LC/MS/MS, this pool of 2-AG is generated via tetrahydrolipstatin-sensitive enzymatic pathways distinct from DAGLalpha or DAGLbeta. Blockade of endocannabinoid hydrolysis by the irreversibly acting inhibitor MAFP evokes CP55,940-mimicking [35S]GTPgammaS binding responses throughout the CB1 receptor enriched brain regions of DAGLalpha-KO, DAGLbeta-KO, and WT mice brain sections. No statistically significant difference is observed in CP55,940-evoked regional CB1 receptor activity between DAGLb-KO and wild-type mice whereas in certain hippocampal regions of DAGLalpha-KO mice (hippocampus-overall, hippocampus-CA3 and hippocampus-dentate gyrus), sub-maximal concentrations of CP55,940 evoke a statistically significant increase in CB1 receptor activity. The observed labelling patterns evoked by both MAFP and CP55,940 are abolished with the CB1 receptor-selective antagonist AM251, confirming that responses are being mediated via the CB1 receptors. Comparison of 2-AG and anandamide (AEA, the other principal endocannabinoid) levels between unprocessed cryosections of DAGLalpha-KO, DAGLbeta-KO and wild-type mice brains
additional information
brain regional CB1 receptor-Gi/o-activity largely remains unaltered in DAGLalpha-knockout and DAGLbeta-knockout mice when compared to wild-type littermates. Following comprehensive pharmacological blockade of 2-AG hydrolysis, brain sections generate sufficient amounts of 2-AG to activate CB1 receptors throughout the regions endowed with these receptors. As demonstrated by LC/MS/MS, this pool of 2-AG is generated via tetrahydrolipstatin-sensitive enzymatic pathways distinct from DAGLalpha or DAGLbeta. Blockade of endocannabinoid hydrolysis by the irreversibly acting inhibitor MAFP evokes CP55,940-mimicking [35S]GTPgammaS binding responses throughout the CB1 receptor enriched brain regions of DAGLalpha-KO, DAGLbeta-KO and WT mice brain sections. No statistically significant difference is observed in CP55,940-evoked regional CB1 receptor activity between DAGLb-KO and wild-type mice whereas in certain hippocampal regions of DAGLalpha-KO mice (hippocampus-overall, hippocampus-CA3, and hippocampus-dentate gyrus), sub-maximal concentrations of CP55,940 evoke a statistically significant increase in CB1 receptor activity. The observed labelling patterns evoked by both MAFP and CP55,940 are abolished with the CB1 receptor-selective antagonist AM251, confirming that responses are being mediated via the CB1 receptors. Comparison of 2-AG and anandamide (AEA, the other principal endocannabinoid) levels between unprocessed cryosections of DAGLalpha-KO, DAGLbeta-KO and wild-type mice brains
additional information
brain regional CB1 receptor-Gi/o-activity largely remains unaltered in DAGLalpha-knockout and DAGLbeta-knockout mice when compared to wild-type littermates. Following comprehensive pharmacological blockade of 2-AG hydrolysis, brain sections generate sufficient amounts of 2-AG to activate CB1 receptors throughout the regions endowed with these receptors. As demonstrated by LC/MS/MS, this pool of 2-AG is generated via tetrahydrolipstatin-sensitive enzymatic pathways distinct from DAGLalpha or DAGLbeta. Blockade of endocannabinoid hydrolysis by the irreversibly acting inhibitor MAFP evokes CP55,940-mimicking [35S]GTPgammaS binding responses throughout the CB1 receptor enriched brain regions of DAGLalpha-KO, DAGLbeta-KO and WT mice brain sections. No statistically significant difference is observed in CP55,940-evoked regional CB1 receptor activity between DAGLb-KO and wild-type mice whereas in certain hippocampal regions of DAGLalpha-KO mice (hippocampus-overall, hippocampus-CA3, and hippocampus-dentate gyrus), sub-maximal concentrations of CP55,940 evoke a statistically significant increase in CB1 receptor activity. The observed labelling patterns evoked by both MAFP and CP55,940 are abolished with the CB1 receptor-selective antagonist AM251, confirming that responses are being mediated via the CB1 receptors. Comparison of 2-AG and anandamide (AEA, the other principal endocannabinoid) levels between unprocessed cryosections of DAGLalpha-KO, DAGLbeta-KO and wild-type mice brains
additional information
construction of DAGLalpha knockout mice. Cholinergic innervation of CA1 pyramidal cells of the hippocampus is sensitive to the genetic disruption of 2-arachidonoylglycerol (2-AG) signaling in DAGLalpha null mice. A hybrid COS-7-cholinergic neuron co-culture system demonstrates that heterologous DAGLalpha overexpression spherically excludes cholinergic growth cones from 2-AG-rich extracellular environments, and minimizes cell-cell contact in vitro. CB1R-mediated exclusion responses lasts 3 days, indicating sustained spherical 2-AG availability. Extracellular 2-AG concentrations can be sufficient to activate CB1Rs along discrete spherical boundaries to modulate neuronal responsiveness. When co-culturing cholinergic neurons and COS-7-DAGLalpha cells for 1-3 days in vitro (DIV), parent COS-7 cells attract cholinergic neurites, which course on or along COS-7 plasmalemmas already by 1 DIV. Accordingly, the distance between cholinergic GCs and the opposing membrane of COS-7 cells gradually decreases as a factor of time. In contrast, 55.0% of cholinergic GCs are prevented from approaching the proximal COS-7 cell's plasmalemma upon DAGLalpha overexpression by 3 DIV. DAGLalpha overexpression spherically excludes cholinergic GCs, as reflected by their significantly increased distance to the surface of COS-7-DAGLalpha cells. DAGLalpha overexpression does not affect the angle at which GCs approach COS-7-DAGLalpha cells, the length of cholinergic neurites, the distance between cholinergic and COS-7 somata, and the survival of p75NTR1 neurons in vitro, excluding delayed morphogenesis or neuronal migration as confounding factors. Yet DAGLalpha overexpression no longer affects neurite growth, confining endocannabinoid action to affecting GC motility but no other forms of e.g. contact guidance. Focal and extracellular 2-AG can alter the positioning of cholinergic GCs. DAGLalpha overexpression in COS-7 cells is the only variable that contributes to the phenomena, supporting a role for intercellular 2-AG signaling
additional information
generation of mutant Daglbeta-/- mice, analysis of the membrane proteome of transiently transfected HEK-293T cells overexpressing mouse DAGLbeta. Using a combination of inhibitors and knockout mice, strong evidence is generated that both DAGLbeta and PLA2G4A contribute to prostaglandin production in lipopolysaccharide-stimulated macrophages
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gene DAGLA, DNA and amino acid sequence determination and analysis, sequence comparisons of the two isozymes, real-time RT-PCR analysis of DAGLalpha expression, recombinant expression of V5- and His-tagged isozyme DAGLalpha in COS-7 cells
gene DAGLA, located on the human chromosome 11q12.2
gene Dagla, stable functional overexpression of V5-tagged DAGLalpha in COS-7 cell membranes, no DAGLalpha-induced change in COS-7 cell morphology or density is observed
gene DAGLalpha, identification of the core promoter region and regulatory elements of DAGLalpha, specificity protein 1 (Sp1), is the only factor that can bind to the GC-box, the core promoter contains both an enhancer and a suppressor region. The GC-box specifically promotes expression in NS cells. Functional transient recombinant expression of pGL3-DAGLalpha promoter constructs plus pRLTK Renilla plasmid in NS cells. Promoter activity study of promoters P1-P11, overview. The full-length DAGLa promoter (P1) is active in Cor-1, CGR8, and NS-5 NS cell lines. A comparative analysis of the eight most relevant promoter constructs in the Cor-1 cells shows that P6 is the smallest and most active promoter. Again, the activity of P6 is suppressed by the 3' region, as revealed with P8, P10, and in this case also P11. The loss of DAGLa promoter luciferase activity in Cor-1 cells is due to a loss of function specific to the GC-box. The core DAGLa promoter is under a different regulatory control in the different cell types and identify two independent elements that can specifically regulate expression in Cor-1 cells. The GC-box is required for DAGLa core promoter activity in Cor-1 cells but not in 3T3 cells
gene DAGLB, DNA and amino acid sequence determination and analysis, sequence comparisons of the two isozymes, recombinant expression of FLAG-tagged isozyme DAGLbeta in COS-7 cells
recombinant expression of DAGLalpha in HEK-293T cells
recombinant expression of the N-terminally GST-tagged catalytic domain (amino acids 228-672, GST-DAGLbeta CD) of DAGLbeta in Spodoptera frugiperda Sf9 insect cells using the baculovirus transfection system. Stable recombinant expression of V5-tagged DAGLbeta (V5beta4) in human U2OS osteosarcoma cells, which are genetically modified to express a CB1 receptor reporter construct (Tango CNR1-bla U2OS cells)
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Ishiguro, H.; Higuchi, S.; Arinami, T.; Onaivi, E.S.
Association between alcoholism and the gene encoding the endocannabinoid synthesizing enzyme diacylglycerol lipase alpha in the Japanese population
Alcohol
68
59-62
2018
Mus musculus (Q6WQJ1), Homo sapiens (Q9Y4D2), Homo sapiens, Mus musculus C57BL/6JJmsSLC (Q6WQJ1)
brenda
Chau, L.; Tai, H.
Release of arachidonate from diglyceride in human platelets requires the sequential action of a diglyceride lipase and a monoglyceride lipase
Biochem. Biophys. Res. Commun.
100
1688-1695
1981
Homo sapiens
brenda
Singh, P.; Markwick, R.; Lu, L.; Howell, F.; Williams, G.; Doherty, P.
Assay and inhibition of the purified catalytic domain of diacylglycerol lipase beta
Biochemistry
55
2713-2721
2016
Homo sapiens (Q8NCG7)
brenda
Aaltonen, N.; Riera Ribas, C.; Lehtonen, M.; Savinainen, J.R.; Laitinen, J.T.
Brain regional cannabinoid CB1 receptor signalling and alternative enzymatic pathways for 2-arachidonoylglycerol generation in brain sections of diacylglycerol lipase deficient mice
Eur. J. Pharm. Sci.
51
87-95
2014
Mus musculus (Q6WQJ1), Mus musculus (Q91WC9)
brenda
Okubo, Y.; Kasamatsu, A.; Yamatoji, M.; Fushimi, K.; Ishigami, T.; Shimizu, T.; Kasama, H.; Shiiba, M.; Tanzawa, H.; Uzawa, K.
Diacylglycerol lipase alpha promotes tumorigenesis in oral cancer by cell-cycle progression
Exp. Cell Res.
367
112-118
2018
Homo sapiens (Q9Y4D2), Homo sapiens
brenda
Bisogno, T.; Howell, F.; Williams, G.; Minassi, A.; Cascio, M.; Ligresti, A.; Matias, I.; Schiano-Moriello, A.; Paul, P.; Williams, E.; Gangadbaran, U.; Hobbs, C.; Di Marzo, V.; Doherty, P.
Cloning of the first sn1-DAG lipases points to the spatial and temporal regulation of endocannabinoid signaling in the brain
J. Cell Biol.
163
463-468
2003
Homo sapiens (Q8NCG7), Homo sapiens (Q9Y4D2)
brenda
Walker, D.; Suetterlin, P.; Reisenberg, M.; Williams, G.; Doherty, P.
Down-regulation of diacylglycerol lipase-alpha during neural stem cell differentiation identification of elements that regulate transcription
J. Neurosci. Res.
88
735-745
2010
Homo sapiens (Q9Y4D2)
brenda
Deng, H.; Van Der Wel, T.; Van Den Berg, R.; Van Den Nieuwendijk, A.; Janssen, F.; Baggelaar, M.; Overkleeft, H.; Van Der Stelt, M.
Chiral disubstituted piperidinyl ureas a class of dual diacylglycerol lipase-alpha and ABHD6 inhibitors
MedChemComm
8
982-988
2017
Mus musculus (Q6WQJ1)
brenda
Bisogno, T.
Assay of DAGLalpha/beta activity
Methods Mol. Biol.
1412
149-156
2016
Mus musculus (Q6WQJ1), Mus musculus (Q91WC9)
brenda
Hsu, K.L.; Tsuboi, K.; Adibekian, A.; Pugh, H.; Masuda, K.; Cravatt, B.F.
DAGLbeta inhibition perturbs a lipid network involved in macrophage inflammatory responses
Nat. Chem. Biol.
8
999-1007
2012
Mus musculus (Q91WC9)
brenda
Keimpema, E.; Alpar, A.; Howell, F.; Malenczyk, K.; Hobbs, C.; Hurd, Y.; Watanabe, M.; Sakimura, K.; Kano, M.; Doherty, P.; Harkany, T.
Diacylglycerol lipase alpha manipulation reveals developmental roles for intercellular endocannabinoid signaling
Sci. Rep.
3
2093
2013
Mus musculus (Q6WQJ1)
brenda