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1 d the crystal structure of the 2-AG isomer 1-arachidonoyl glycerol (1-AG) in complex with wild type a
2  (LTD) was mediated by the endocannabinoid 2-arachidonoyl glycerol (2-AG) acting on a TRPV (transient
3 genation of endogenous cannabinoids (eCBs) 2-arachidonoyl glycerol (2-AG) and arachidonoyl ethanolami
4 The endocannabinoids (eCBs) anandamide and 2-arachidonoyl glycerol (2-AG) are inactivated by a two-st
5 ith elevated levels of the endocannabinoid 2-arachidonoyl glycerol (2-AG) are protected from enteric
6  the endocannabinoids anandamide (AEA) and 2-arachidonoyl glycerol (2-AG) are released by aversive tr
7  Bean (2017) show that the endocannabinoid 2-arachidonoyl glycerol (2-AG) can directly alter the prop
8 or agonist WIN55212-2 (10-30 ng/side), the 2-arachidonoyl glycerol (2-AG) hydrolysis inhibitor JZL184
9 drolase-induced increases in anandamide or 2-arachidonoyl glycerol (2-AG) levels, resulting in analge
10 exposure paradigms increased VTA dialysate 2-arachidonoyl glycerol (2-AG) levels.
11 n this study, we determined the effects of 2-arachidonoyl glycerol (2-AG) on hepatic stellate cells (
12 effects of endogenous anandamide (AEA) and 2-arachidonoyl glycerol (2-AG) on the permeability and inf
13 , and spinal cord levels of anandamide and 2-arachidonoyl glycerol (2-AG) were increased in MIA-treat
14 damide (arachidonoylethanolamide, AEA) and 2-arachidonoyl glycerol (2-AG), and of the AEA congener, p
15 in endogenous cannabinoids, anandamide and 2-arachidonoyl glycerol (2-AG), are produced on demand fro
16 ain endocannabinoids, anandamide (AEA) and 2-arachidonoyl glycerol (2-AG), are released in an activit
17  is itself occluded by the endocannabinoid 2-arachidonoyl glycerol (2-AG), consistent with 2-AG as a
18 or agonists, including the endocannabinoid 2-arachidonoyl glycerol (2-AG), for [35S]GTPgammaS binding
19              Endocannabinoid, particularly 2-arachidonoyl glycerol (2-AG), signaling has recently eme
20 eleases high levels of the endocannabinoid 2-arachidonoyl glycerol (2-AG), suggesting an alternative
21 he two eCB molecules, anandamide (AEA) and 2-arachidonoyl glycerol (2-AG), with stress exposure reduc
22 ades since the discovery of anandamide and 2-arachidonoyl glycerol (2-AG).
23 e production of the endogenous cannabinoid 2-arachidonoyl glycerol (2-AG).
24 nts, i.e., free AA and the endocannabinoid 2-arachidonoyl glycerol (2-AG).
25 nate endocannabinoid substrates, including 2-arachidonoyl glycerol (2-AG).
26 egulated hydrolysis of the endocannabinoid 2-arachidonoyl glycerol (2-AG).
27  after incubation with the endocannabinoid 2-arachidonoyl glycerol (2-AG).
28 ), implicated in the production of the eCB 2-arachidonoyl glycerol (2-AG); monoacylglycerol lipase (M
29                     Endocannabinoid (eCB), 2-arachidonoyl-glycerol (2-AG), the most abundant eCB in t
30 nctions as the main metabolizing enzyme of 2-arachidonoyl glycerol, an endocannabinoid signaling lipi
31                                            2-Arachidonoyl glycerol, an endocannabinoid, is one such m
32 ndothelin-1 with the putative vasorelaxant 2-arachidonoyl glycerol, an endogenous cannabimimetic deri
33 espite similarities in chemical structure, 2-arachidonoyl glycerol and anandamide are synthesized and
34 n the CNS, early-life stress (1) decreased 2-arachidonoyl glycerol and arachidonic acid in the cerebe
35 e best-studied endogenous cannabinoids are 2-arachidonoyl glycerol and arachidonoyl ethanolamide (ana
36                       The endocannabinoids 2-arachidonoyl-glycerol and N-arachidonoyl-ethanolamine me
37 arachidonoyl ethanolamide (anandamide) and 2-arachidonoyl glycerol, and the plant-derived Delta(9)-te
38 cts of the endocannabinoids anandamide and 2-arachidonoyl glycerol are terminated by enzymatic hydrol
39 city of molecular rearrangements impairing 2-arachidonoyl glycerol availability and actions may diffe
40   In addition, we found that inhibition of 2-arachidonoyl glycerol biosynthesis blocked LTD induction
41 r example, N-arachidonoyl-ethanolamine and 2-arachidonoyl-glycerol can be metabolized by cyclooxygena
42               This study demonstrates that 2-arachidonoyl glycerol counteracts Ca(2+) mobilization an
43 e fatty acid amide hydrolase; or the 2-AG (2-arachidonoyl glycerol)-degrading enzyme monoacylglycerol
44 e fatty acid amide hydrolase; or the 2-AG (2-arachidonoyl glycerol)-degrading enzyme monoacylglycerol
45    We found that microglia, expressing two 2-arachidonoyl glycerol-degrading enzymes, serine hydrolas
46 ents, secoisolariciresinol diglucoside and 2-arachidonoyl glycerol, demonstrated protection by reduci
47 situs nucleus in males only; (2) decreased 2-arachidonoyl glycerol in females only in cerebellar Crus
48                                        The 2-arachidonoyl glycerol-induced phosphorylation of vasodil
49 sis blocked LTD induction, suggesting that 2-arachidonoyl glycerol is the most likely retrograde eCB
50 wo endocannabinoids, such as anandamide or 2-arachidonoyl glycerol, is insufficient to describe the b
51                These findings suggest that 2-arachidonoyl glycerol may contribute to the regulation o
52 have experimentally confirmed that altered 2-arachidonoyl glycerol signalling could contribute to syn
53     We hypothesized that errant retrograde 2-arachidonoyl glycerol signalling impairs synaptic neurot
54 sease progression slows the termination of 2-arachidonoyl glycerol signalling.
55 pase alpha and beta isoforms, synthesizing 2-arachidonoyl glycerol, significantly increased in defini
56 f endogenous levels of AEA, and, possibly, 2-arachidonoyl glycerol-significantly ameliorated spastici
57  potency, and efficacy of meth-anandamide, 2-arachidonoyl glycerol, virodhamine, Noladin ether, docos
58 or endogenous cannabinoids (anandamide and 2-arachidonoyl glycerol) were identified only 20 to 25 yea
59 nnabinoids, N-arachidonoylethanolamine and 2-arachidonoyl-glycerol, which derive from arachidonic aci