ライフサイエンスコーパス: monoacylglycerol lipase

1 reased expression of its degradative enzyme, monoacylglycerol lipase.

2 se and alpha/beta-hydrolase domain 6 but not monoacylglycerol lipase.

3 ted activity should be viewed as an esterase-monoacylglycerol lipase.

4 Here, monoacylglycerol lipase accumulates in CB(1) cannabinoid

5 ng phospholipase A, lysophospholipase A, and monoacylglycerol lipase, although they are potential can

6 6, abhydrolase domain-containing protein 12, monoacylglycerol lipase, and fatty acid amide hydrolase

7 These studies also identify monoacylglycerol lipase as a previously unrecognized the

8 alpha/beta-hydrolase domain-containing 6 and monoacylglycerol lipase, begin to surround senile plaque

9 ls containing hyperphosphorylated tau retain monoacylglycerol lipase expression, although at levels s

10 alpha/beta-hydrolase domain-containing 6 and monoacylglycerol lipase in hippocampal neurons: serine h

11 achidonoylglycerol (2-AG) degradation enzyme monoacylglycerol lipase, indicating that it is mediated

12 increases in 2-AG levels obtained following monoacylglycerol lipase inhibition.

13 th GAT211, but it was not preserved with the monoacylglycerol lipase inhibitor JZL184.

14 Indeed, the specific monoacylglycerol lipase inhibitor URB602 prevented Trans

15 erone, the CB1R agonist WIN 55,212-2, or the monoacylglycerol lipase inhibitor URB602.

16 cid amide hydrolase inhibitor) and JZL184 (a monoacylglycerol lipase inhibitor).

17 effects with fatty acid amide hydrolase and monoacylglycerol lipase inhibitors in paclitaxel-treated

18 lipases, including hormone-sensitive lipase, monoacylglycerol lipase, lipoprotein lipase, and patatin

19 work we report a new series of inhibitors of monoacylglycerol lipase (MAGL) and fatty acid amide hydr

20 Monoacylglycerol lipase (MAGL) and fatty acid amide hydr

21 a et al. now demonstrate that an increase in monoacylglycerol lipase (MAGL) drives tumorigenesis thro

22 at a distinct pathway exists in brain, where monoacylglycerol lipase (MAGL) hydrolyzes the endocannab

23 fects of both systemic pretreatment with the monoacylglycerol lipase (MAGL) inhibitor MJN110 (which s

24 Monoacylglycerol lipase (MAGL) inhibitors are considered

25 recent years in developing selective, potent monoacylglycerol lipase (MAGL) inhibitors.

26 Here, we show that the enzyme monoacylglycerol lipase (MAGL) is highly expressed in ag

27 Monoacylglycerol lipase (MAGL) is responsible for signal

28 Monoacylglycerol lipase (MAGL) links these pathways, hyd

29 on of the endocannabinoid catabolic enzymes, monoacylglycerol lipase (MAGL) or fatty acid amide hydro

30 Monoacylglycerol lipase (MAGL) represents a primary degr

31 JZL184, a potent and selective inhibitor for monoacylglycerol lipase (MAGL) that hydrolyzes 2-AG, ind

32 enzymatic hydrolysis, mainly carried out by monoacylglycerol lipase (MAGL), along with a small contr

33 l lipase (DAGL) or the 2-AG-degrading enzyme monoacylglycerol lipase (MAGL), and assessing the therap

34 either fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL), enzymes that regulate th

35 including fatty acid amide hydrolase (FAAH), monoacylglycerol lipase (MAGL), N-acylethanolamine acid

36 the antidepressant actions of inhibitors of monoacylglycerol lipase (MAGL), the major degradative en

37 We showed previously that inhibition of monoacylglycerol lipase (MAGL), the primary enzyme that

38 sm was produced by sustained inactivation of monoacylglycerol lipase (MAGL), the principal degradativ

39 the authors show that genetic disruption of monoacylglycerol lipase (MAGL), the principal degradativ

40 2-AG is degraded primarily by monoacylglycerol lipase (MAGL), which is expressed in ne

41 L), which biosynthesizes 2-AG, inhibition of monoacylglycerol lipase (MAGL), which metabolizes 2-AG,

42 rachidonoylglycerol (2-AG) is inactivated by monoacylglycerol lipase (MAGL).

43 ylglycerol (2-AG) is hydrolysed primarily by monoacylglycerol lipase (MAGL).

44 ylglycerol (2-AG) is hydrolyzed primarily by monoacylglycerol lipase (MAGL).

45 hydrolyzed primarily by the serine hydrolase monoacylglycerol lipase (MAGL).

46 yzing enzyme ABHD6 (intracellular WWL70) and monoacylglycerol lipase MGL (JZL184) or by blocking GABA

47 n of the eCB 2-arachidonoyl glycerol (2-AG); monoacylglycerol lipase (MGL) and alpha/beta-hydrolase d

48 sted whether PG-G levels may be regulated by monoacylglycerol lipase (MGL) and fatty acid amide hydro

49 The serine hydrolase monoacylglycerol lipase (MGL) functions as the main meta

50 ydrolysis and demonstrated expression of the monoacylglycerol lipase (MGL) gene in human intestinal C

51 y of compound 4a, a potent beta-lactam-based monoacylglycerol lipase (MGL) inhibitor characterized by

52 have shown previously that overexpression of monoacylglycerol lipase (MGL), a cytosolic serine hydrol

53 The function of monoacylglycerol lipase (MGL), a key actor in the hydrol

54 hydrolase (FAAH), cyclooxygenase-2 (COX-2), monoacylglycerol lipase (MGL), and alpha/beta-hydrolase

55 ju3p, the functional orthologue of mammalian monoacylglycerol lipase (MGL), contributes >90% of cellu

56 In doing so, NGF limits the sorting of monoacylglycerol lipase (MGL), rate limiting 2-AG bioava

57 Furthermore, we show that astrocytes express monoacylglycerol lipase (MGL), the main hydrolyzing enzy

58 temic or local pharmacological inhibition of monoacylglycerol lipase (MGL)-a lipid hydrolase that deg

59 atty acid amide hydrolase (FAAH) and 2-AG by monoacylglycerol lipase (MGL).

60 Monoacylglycerol lipases (MGLs) play an important role i

61 r, inhibition of the eCB deactivating enzyme monoacylglycerol lipase normalized eCB-LTD in mBACtgDyrk

62 ating enzymes fatty acid amide hydrolase and monoacylglycerol lipase produce reliable antinociceptive

63 Subcellular fractionation revealed impaired monoacylglycerol lipase recruitment to biological membra

64 Enzymes that hydrolyze 2-AG, such as monoacylglycerol lipase, regulate the accumulation and e

65 d inhibitor of the 2-AG-deactivating enzyme, monoacylglycerol lipase, selectively increases 2-AG conc

66 tion enzymes, fatty acid amid hydrolase, and monoacylglycerol lipase than males, and lower amounts of

67 se activity while inhibiting the activity of monoacylglycerol lipase, the enzyme that degrades 2-AG.

68 This inverse sensitivity of DG lipase and monoacylglycerol lipase to calcium constitutes an origin

69 and possibly the enzymes diacylglycerol and monoacylglycerol lipases to yield free AA.

70 a potent reversible inhibitor of the enzyme monoacylglycerol lipase, which accounts for 85% of the 2

71 a potent reversible inhibitor of the enzyme monoacylglycerol lipase, which accounts for 85% of the 2