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1 G (2-arachidonoyl glycerol)-degrading enzyme monoacylglycerol lipase.
2 G (2-arachidonoyl glycerol)-degrading enzyme monoacylglycerol lipase.
3 increased degradation of endocannabinoids by monoacylglycerol lipase.
4 reased expression of its degradative enzyme, monoacylglycerol lipase.
5 se and alpha/beta-hydrolase domain 6 but not monoacylglycerol lipase.
6 ted activity should be viewed as an esterase-monoacylglycerol lipase.
7 e (ATGL) and not hormone-sensitive lipase or monoacylglycerol lipase.
8 es showed that pharmacological inhibition of monoacylglycerol lipase, a key enzyme degrading the endo
9                                        Here, monoacylglycerol lipase accumulates in CB(1) cannabinoid
10 ng phospholipase A, lysophospholipase A, and monoacylglycerol lipase, although they are potential can
11 6, abhydrolase domain-containing protein 12, monoacylglycerol lipase, and fatty acid amide hydrolase
12                  These studies also identify monoacylglycerol lipase as a previously unrecognized the
13     In contrast, pharmacologic inhibition of monoacylglycerol lipase attenuates GBM proliferation.
14 alpha/beta-hydrolase domain-containing 6 and monoacylglycerol lipase, begin to surround senile plaque
15                                              Monoacylglycerol lipase deficiency affects diet-induced
16 ls containing hyperphosphorylated tau retain monoacylglycerol lipase expression, although at levels s
17                          Inhibition of human Monoacylglycerol Lipase (hMGL) offers a novel approach f
18 alpha/beta-hydrolase domain-containing 6 and monoacylglycerol lipase in hippocampal neurons: serine h
19 protective effects produced by inhibition of monoacylglycerol lipase in traumatic brain injury remain
20 nalling in astrocytes is responsible for the monoacylglycerol lipase inactivation-produced alleviatio
21                                          The monoacylglycerol lipase inactivation-produced neuroprote
22 achidonoylglycerol (2-AG) degradation enzyme monoacylglycerol lipase, indicating that it is mediated
23      This study shows an additive mechanism (monoacylglycerol lipase inhibition) by which BCP might i
24  increases in 2-AG levels obtained following monoacylglycerol lipase inhibition.
25 th GAT211, but it was not preserved with the monoacylglycerol lipase inhibitor JZL184.
26                         Indeed, the specific monoacylglycerol lipase inhibitor URB602 prevented Trans
27 erone, the CB1R agonist WIN 55,212-2, or the monoacylglycerol lipase inhibitor URB602.
28 cid amide hydrolase inhibitor) and JZL184 (a monoacylglycerol lipase inhibitor).
29 augmentation via administration of JZL184, a monoacylglycerol lipase inhibitor, blocked SI deficits a
30  enzyme that reacts potently with a covalent monoacylglycerol lipase inhibitor.
31  effects with fatty acid amide hydrolase and monoacylglycerol lipase inhibitors in paclitaxel-treated
32 l RNA-sequencing data reveal that astrocytic monoacylglycerol lipase knockout mice display greater re
33 lipases, including hormone-sensitive lipase, monoacylglycerol lipase, lipoprotein lipase, and patatin
34                                              Monoacylglycerol lipase (MAGL) activity was evaluated in
35 work we report a new series of inhibitors of monoacylglycerol lipase (MAGL) and fatty acid amide hydr
36                                              Monoacylglycerol lipase (MAGL) and fatty acid amide hydr
37 ppression of inhibition (DSI) was limited by monoacylglycerol lipase (MAGL) but not by fatty acid ami
38 a et al. now demonstrate that an increase in monoacylglycerol lipase (MAGL) drives tumorigenesis thro
39 ntly associated with regional differences in monoacylglycerol lipase (MAGL) expression in postmortem
40 at a distinct pathway exists in brain, where monoacylglycerol lipase (MAGL) hydrolyzes the endocannab
41  2-arachidonoylglycerol with a low dose of a monoacylglycerol lipase (MAGL) inhibitor facilitates mot
42         Inhibiting 2-AG degradation with the monoacylglycerol lipase (MAGL) inhibitor JZL184 during i
43 fects of both systemic pretreatment with the monoacylglycerol lipase (MAGL) inhibitor MJN110 (which s
44                                              Monoacylglycerol lipase (MAGL) inhibitors are considered
45                        New potent, selective monoacylglycerol lipase (MAGL) inhibitors based on the a
46 recent years in developing selective, potent monoacylglycerol lipase (MAGL) inhibitors.
47                                              Monoacylglycerol lipase (MAGL) is a hydrolase involved i
48                                              Monoacylglycerol lipase (MAGL) is a key enzyme involved
49                Here, we show that the enzyme monoacylglycerol lipase (MAGL) is highly expressed in ag
50                                              Monoacylglycerol lipase (MAGL) is one of the key enzymes
51                                              Monoacylglycerol lipase (MAGL) is responsible for signal
52                                              Monoacylglycerol lipase (MAGL) is the enzyme degrading t
53                                              Monoacylglycerol lipase (MAGL) is the enzyme responsible
54                                              Monoacylglycerol lipase (MAGL) is the key enzyme for the
55                                              Monoacylglycerol lipase (MAGL) is the pivotal catabolic
56                                              Monoacylglycerol lipase (MAGL) links these pathways, hyd
57 on of the endocannabinoid catabolic enzymes, monoacylglycerol lipase (MAGL) or fatty acid amide hydro
58                                              Monoacylglycerol lipase (MAGL) regulates endocannabinoid
59                                              Monoacylglycerol lipase (MAGL) represents a primary degr
60 JZL184, a potent and selective inhibitor for monoacylglycerol lipase (MAGL) that hydrolyzes 2-AG, ind
61 recent efforts have focused on inhibition of monoacylglycerol lipase (MAGL) to enhance signaling of t
62 n addition, a series of tetrazine probes for monoacylglycerol lipase (MAGL) were synthesized and the
63                                Inhibition of monoacylglycerol lipase (MAGL) with JZL184 increases the
64                                              Monoacylglycerol lipase (MAGL), a serine hydrolase exten
65  enzymatic hydrolysis, mainly carried out by monoacylglycerol lipase (MAGL), along with a small contr
66 l lipase (DAGL) or the 2-AG-degrading enzyme monoacylglycerol lipase (MAGL), and assessing the therap
67 ological inhibition of its catabolic enzyme, monoacylglycerol lipase (MAGL), either systemically or i
68  either fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL), enzymes that regulate th
69 including fatty acid amide hydrolase (FAAH), monoacylglycerol lipase (MAGL), N-acylethanolamine acid
70  the antidepressant actions of inhibitors of monoacylglycerol lipase (MAGL), the major degradative en
71      We showed previously that inhibition of monoacylglycerol lipase (MAGL), the primary enzyme that
72 sm was produced by sustained inactivation of monoacylglycerol lipase (MAGL), the principal degradativ
73  the authors show that genetic disruption of monoacylglycerol lipase (MAGL), the principal degradativ
74  novel transcriptional target MGLL, encoding monoacylglycerol lipase (MAGL), to regulate the self-ren
75                2-AG is degraded primarily by monoacylglycerol lipase (MAGL), which is expressed in ne
76 L), which biosynthesizes 2-AG, inhibition of monoacylglycerol lipase (MAGL), which metabolizes 2-AG,
77 18)F]YH134 as a novel PET tracer for imaging monoacylglycerol lipase (MAGL).
78 n 5 (FABP5), fatty acid synthase (FASN), and monoacylglycerol lipase (MAGL).
79 rachidonoylglycerol (2-AG) is inactivated by monoacylglycerol lipase (MAGL).
80 ylglycerol (2-AG) is hydrolysed primarily by monoacylglycerol lipase (MAGL).
81 ylglycerol (2-AG) is hydrolyzed primarily by monoacylglycerol lipase (MAGL).
82 hydrolyzed primarily by the serine hydrolase monoacylglycerol lipase (MAGL).
83 yzing enzyme ABHD6 (intracellular WWL70) and monoacylglycerol lipase MGL (JZL184) or by blocking GABA
84 n of the eCB 2-arachidonoyl glycerol (2-AG); monoacylglycerol lipase (MGL) and alpha/beta-hydrolase d
85 iators of the inflammatory response, such as monoacylglycerol lipase (MGL) and fatty acid amide hydro
86 sted whether PG-G levels may be regulated by monoacylglycerol lipase (MGL) and fatty acid amide hydro
87                         The serine hydrolase monoacylglycerol lipase (MGL) functions as the main meta
88 ydrolysis and demonstrated expression of the monoacylglycerol lipase (MGL) gene in human intestinal C
89 y of compound 4a, a potent beta-lactam-based monoacylglycerol lipase (MGL) inhibitor characterized by
90                                              Monoacylglycerol lipase (MGL) is the last enzymatic step
91 have shown previously that overexpression of monoacylglycerol lipase (MGL), a cytosolic serine hydrol
92                              The function of monoacylglycerol lipase (MGL), a key actor in the hydrol
93 e in high-fat diet (HFD)-induced obesity for monoacylglycerol lipase (MGL), an enzyme that is also kn
94  hydrolase (FAAH), cyclooxygenase-2 (COX-2), monoacylglycerol lipase (MGL), and alpha/beta-hydrolase
95 ju3p, the functional orthologue of mammalian monoacylglycerol lipase (MGL), contributes >90% of cellu
96       In doing so, NGF limits the sorting of monoacylglycerol lipase (MGL), rate limiting 2-AG bioava
97                                Inhibitors of monoacylglycerol lipase (MGL), the enzyme that deactivat
98 Furthermore, we show that astrocytes express monoacylglycerol lipase (MGL), the main hydrolyzing enzy
99 Z) derivatives that are potent inhibitors of monoacylglycerol lipase (MGL), the primary degrading enz
100 temic or local pharmacological inhibition of monoacylglycerol lipase (MGL)-a lipid hydrolase that deg
101 atty acid amide hydrolase (FAAH) and 2-AG by monoacylglycerol lipase (MGL).
102 d eicosanoid lipids by DAG lipase (DAGL) and monoacylglycerol lipase (MGLL) enzymes in innate immune
103 h expression of the serine hydrolase enzymes monoacylglycerol lipase (MGLL) or carboxylesterase 1 (CE
104                                              Monoacylglycerol lipases (MGLs) play an important role i
105 r, inhibition of the eCB deactivating enzyme monoacylglycerol lipase normalized eCB-LTD in mBACtgDyrk
106 ating enzymes fatty acid amide hydrolase and monoacylglycerol lipase produce reliable antinociceptive
107  Subcellular fractionation revealed impaired monoacylglycerol lipase recruitment to biological membra
108  Here we first show that genetic deletion of monoacylglycerol lipase reduces neuropathology and avert
109         Enzymes that hydrolyze 2-AG, such as monoacylglycerol lipase, regulate the accumulation and e
110 d inhibitor of the 2-AG-deactivating enzyme, monoacylglycerol lipase, selectively increases 2-AG conc
111 c (10 days) JZL184, a selective inhibitor of monoacylglycerol lipase, specifically normalized the soc
112 oscopy to selectively activate intracellular monoacylglycerol lipase tagged with DHTz-labeled small m
113 tion enzymes, fatty acid amid hydrolase, and monoacylglycerol lipase than males, and lower amounts of
114 t neurons are rescued by inhibition of MGLL (monoacylglycerol lipase), the enzyme responsible for 2-A
115 se activity while inhibiting the activity of monoacylglycerol lipase, the enzyme that degrades 2-AG.
116    This inverse sensitivity of DG lipase and monoacylglycerol lipase to calcium constitutes an origin
117  and possibly the enzymes diacylglycerol and monoacylglycerol lipases to yield free AA.
118  a potent reversible inhibitor of the enzyme monoacylglycerol lipase, which accounts for 85% of the 2
119  a potent reversible inhibitor of the enzyme monoacylglycerol lipase, which accounts for 85% of the 2

 
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