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1 ty and expression of the OEAdegrading enzyme fatty acid amide hydrolase.
2 1.80 fmol/mg protein) that is distinct from fatty acid amide hydrolase.
3 entiation of the anandamide catabolic enzyme fatty acid amide hydrolase.
4 ivity of the anandamide-catabolizing enzyme, fatty acid amide hydrolase.
5 e than N-arachidonoylserotonin in inhibiting fatty acid amide hydrolase.
6 y of the endocannabinoid metabolizing enzyme fatty acid amide hydrolase.
7 transporter while being a poor substrate for fatty-acid amide hydrolase.
8 tion of arachidonic acid and ethanolamine by fatty-acid amide hydrolase.
9 he intracellular anandamide-degrading enzyme fatty acid amide hydrolase-1 (FAAH-1), termed FAAH-like
11 EA synthesis, without concomitant changes in fatty acid amide hydrolase, an enzyme responsible for OE
13 pharmacological profile in that it inhibits fatty acid amide hydrolase and alpha/beta-hydrolase doma
14 ing protein 12, monoacylglycerol lipase, and fatty acid amide hydrolase and did not display affinity
15 duced synergistic antiallodynic effects with fatty acid amide hydrolase and monoacylglycerol lipase i
16 bitors of endocannabinoid-regulating enzymes fatty acid amide hydrolase and monoacylglycerol lipase p
17 verall, the MAH data are similar to those of fatty acid amide hydrolase and support the suggestion th
18 availability of the X-ray structures of Pam, fatty acid amide hydrolase, and malonamidase E2 has led
19 udies revealed that NAPE-phospholipase D and fatty acid amide hydrolase are expressed in intestinal e
20 s of NAGly and its degradation by the enzyme fatty acid amide hydrolase can be observed in rat brain
22 Preventing their degradation (by inhibiting fatty acid amide hydrolase) enhanced the effects of OEA
23 rgan radiation exposure for the irreversible fatty acid amide hydrolase enzyme probe (11)C-CURB is wi
24 Here we show that mice lacking the enzyme fatty acid amide hydrolase (FAAH(-/-)) are severely impa
25 ates a common human mutation in the gene for fatty acid amide hydrolase (FAAH) (C385A; rs324420), the
26 aint stress, which results in an increase in fatty acid amide hydrolase (FAAH) activity and a reducti
29 el fluorescent assay to continuously monitor fatty acid amide hydrolase (FAAH) activity that is simpl
30 cells, and then anandamide is hydrolyzed by fatty acid amide hydrolase (FAAH) and 2-AG by monoacylgl
31 paradigm to exert combined activity at human fatty acid amide hydrolase (FAAH) and dopamine receptor
32 rotein that may modulate CB(1) function; and fatty acid amide hydrolase (FAAH) and N-acylethanolamine
33 hibitors 3-5 bound to a humanized variant of fatty acid amide hydrolase (FAAH) are disclosed and comp
35 c enzymes, monoacylglycerol lipase (MAGL) or fatty acid amide hydrolase (FAAH) attenuates naloxone-pr
41 dized by lipoxygenase (LOX) or hydrolyzed by fatty acid amide hydrolase (FAAH) during normal seedling
43 he action of diverse hydrolases, among which fatty acid amide hydrolase (FAAH) has been well characte
45 tigated the role of the AEA-degrading enzyme fatty acid amide hydrolase (FAAH) in AEA-induced cell de
46 holipase D (NAPE-PLD) and its degradation by fatty acid amide hydrolase (FAAH) in mouse embryos and o
47 holipase D (NAPE-PLD) and its degradation by fatty acid amide hydrolase (FAAH) in mouse embryos and o
48 ain lipids regulated by the mammalian enzyme fatty acid amide hydrolase (FAAH) in vivo, including kno
54 l finding that posttraining infusions of the fatty acid amide hydrolase (FAAH) inhibitor URB597, whic
57 nd characterization of alpha-ketoheterocycle fatty acid amide hydrolase (FAAH) inhibitors are disclos
58 nd urea derivatives are important classes of fatty acid amide hydrolase (FAAH) inhibitors that carbam
73 evels of endocannabinoids with inhibitors of fatty acid amide hydrolase (FAAH) is analgesic in models
77 y-state time points (5 min), suggesting that fatty acid amide hydrolase (FAAH) may be responsible for
78 liana, and they can be metabolized by either fatty acid amide hydrolase (FAAH) or by lipoxygenase (LO
79 cal inhibition or genetic deletion of either fatty acid amide hydrolase (FAAH) or monoacylglycerol li
81 ngle nucleotide polymorphisms CNR1 rs806378, fatty acid amide hydrolase (FAAH) rs324420, and MGLL rs4
83 were prepared and examined as inhibitors of fatty acid amide hydrolase (FAAH) that additionally targ
85 eral principle, the serine hydrolytic enzyme fatty acid amide hydrolase (FAAH) was found to degrade a
87 rease in side population (SP) cells, whereas fatty acid amide hydrolase (FAAH)(-/-) mice, which have
89 azole inhibitors (1 (OL-135) and 2) bound to fatty acid amide hydrolase (FAAH), a key enzymatic regul
90 ce of the eCB N-arachidonoylethanolamine via fatty acid amide hydrolase (FAAH), although it is unclea
93 l structure of the integral membrane protein fatty acid amide hydrolase (FAAH), an enzyme that degrad
94 endocytosis, and finally, to be degraded by fatty acid amide hydrolase (FAAH), an integral membrane
95 ting that following metabolism by the enzyme fatty acid amide hydrolase (FAAH), anandamide metabolite
96 endocannabinoid anandamide is hydrolysis by fatty acid amide hydrolase (FAAH), and inhibitors of the
97 erminated following hydrolysis by 2 enzymes: fatty acid amide hydrolase (FAAH), and the less-studied
98 L activity as well as their selectivity over fatty acid amide hydrolase (FAAH), another endocannabino
99 mes have been considered to serve this role: fatty acid amide hydrolase (FAAH), cyclooxygenase-2 (COX
101 nships of 2b (OL-135), a potent inhibitor of fatty acid amide hydrolase (FAAH), is detailed targeting
102 (SAR) of 2f (OL-135), a potent inhibitor of fatty acid amide hydrolase (FAAH), is detailed, targetin
103 ated by several metabolic enzymes, including fatty acid amide hydrolase (FAAH), monoacylglycerol lipa
104 inhibition of cyclooxygenase-2 (COX-2), not fatty acid amide hydrolase (FAAH), prolongs DSI, suggest
105 on, cloning, and expression of a rat enzyme, fatty acid amide hydrolase (FAAH), that degrades bioacti
106 incipal endocannabinoid-inactivating enzyme, fatty acid amide hydrolase (FAAH), that in homozygous fo
108 opment of exceptionally potent inhibitors of fatty acid amide hydrolase (FAAH), the enzyme responsibl
109 eripherally restricted inhibitor (URB937) of fatty acid amide hydrolase (FAAH), the enzyme responsibl
110 issense variant Pro129Thr of the gene coding fatty acid amide hydrolase (FAAH), the major degrading e
111 cluding the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH), triacylglycerol hydro
112 inhibition of endocannabinoid transport and fatty acid amide hydrolase (FAAH), two mechanisms of end
113 ignaling related to a common polymorphism in fatty acid amide hydrolase (FAAH), which alters endocann
114 HR1), evokes a rapid induction of the enzyme fatty acid amide hydrolase (FAAH), which causes a reduct
115 that promotes the cellular uptake of AEA and fatty acid amide hydrolase (FAAH), which hydrolyzes AEA
116 g activity is terminated by an enzyme called fatty acid amide hydrolase (FAAH), which hydrolyzes NAEs
117 bition of endocannabinoid hydrolyzing enzyme fatty acid amide hydrolase (FAAH), which leads to increa
118 hypoxic pulmonary vasoconstriction (HPV) via fatty acid amide hydrolase (FAAH)-dependent metabolites.
119 d 2-arachidonylglycerol) degradative enzyme, fatty acid amide hydrolase (FAAH)-IR, in the rat retina.
120 t negative growth-regulating properties, and fatty acid amide hydrolase (FAAH)-mediated hydrolysis is
139 in those cells containing an amidase called fatty-acid amide hydrolase (FAAH) is hydrolysis to arach
140 internalization, anandamide is hydrolyzed by fatty-acid amide hydrolase (FAAH), an intracellular memb
142 dentified at the molecular level (designated fatty acid amide hydrolase, FAAH), and although an analo
143 chemically and described as an inhibitor of fatty acid amide hydrolase, had previously been found in
145 ill hereafter refer to oleamide hydrolase as fatty-acid amide hydrolase, in recognition of the plural
146 pathways can be suggested: 1) inhibition of fatty acid amide hydrolase-induced increases in anandami
147 modulation of emotional states and point to fatty acid amide hydrolase inhibition as an innovative a
149 ibiting their metabolizing enzymes URB597 (a fatty acid amide hydrolase inhibitor) and JZL184 (a mono
152 e phytocannabinoid cannabidiol and selective fatty acid amide hydrolase inhibitors has been proposed,
156 ve MAGL inhibitor JZL184, in Mgll(-/-) mice, fatty acid amide hydrolase(-/-) mice, and in cannabinoid
158 AEs are hydrolyzed intracellularly by either fatty acid amide hydrolase or N-acylethanolamine-hydroly
159 cerol lipase paralogs (DAGLalpha, DAGLbeta), fatty acid amide hydrolase paralogs (FAAH1, FAAH2), mono
160 sion of the Arabidopsis NAE degrading enzyme fatty acid amide hydrolase resulted in seedlings that we
161 oxylipin metabolites were identified in FAAH fatty acid amide hydrolase seedlings but not in wild-typ
162 also show that dCAD cells express functional fatty acid amide hydrolase, the enzyme primarily respons
163 ective and systemically active inhibitors of fatty acid amide hydrolase, the enzyme responsible for t
164 th as oleamide agonists and as inhibitors of fatty acid amide hydrolase, which is responsible for the
165 bitors of the anandamide-deactivating enzyme fatty-acid amide hydrolase, which selectively elevate an
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