PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
24671573-2	2014	In the present study, we show that the application of the endocannabinoids (eCBs) 2-arachidonoylglycerol (2-AG) and methanandamide [a stable analog of the eCB anandamide (AEA)] can activate CB2Rs of mPFC layer II/III pyramidal neurons, which subsequently induces a Cl(-) current.	aea	171-174	cannabinoid receptor 2	Rattus norvegicus	190-193
25519724-2	2015	Accordingly, inhibition of fatty acid amide hydrolase (FAAH), a degrading enzyme of the endocannabinoids N-arachidonoylethanolamine (anandamide; AEA) and 2-arachidonoylglycerol (2-AG) as well as of the endocannabinoid-like substances N-oleoylethanolamine (OEA) and N-palmitoylethanolamine (PEA), can cause augmented endogenous cannabinoid tone.	aea	105-131	fatty acid amide hydrolase	Homo sapiens	55-59
25041240-7	2014	This AEA-induced suppression of inhibition was enhanced by the fatty acid amide hydrolase (FAAH) inhibitor, URB597, whereas a 2-AG-induced suppression of inhibition was unmasked by the monoacylglycerol lipase (MGL) inhibitor, JZL184.	aea	5-8	fatty-acid amide hydrolase-like	Rattus norvegicus	63-89
25041240-7	2014	This AEA-induced suppression of inhibition was enhanced by the fatty acid amide hydrolase (FAAH) inhibitor, URB597, whereas a 2-AG-induced suppression of inhibition was unmasked by the monoacylglycerol lipase (MGL) inhibitor, JZL184.	aea	5-8	fatty-acid amide hydrolase-like	Rattus norvegicus	91-95
25041240-7	2014	This AEA-induced suppression of inhibition was enhanced by the fatty acid amide hydrolase (FAAH) inhibitor, URB597, whereas a 2-AG-induced suppression of inhibition was unmasked by the monoacylglycerol lipase (MGL) inhibitor, JZL184.	aea	5-8	monoglyceride lipase	Rattus norvegicus	210-213
25041240-10	2014	These actions of AEA and 2-AG are tightly regulated by their respective degradative enzymes, FAAH and MGL.	aea	17-20	fatty-acid amide hydrolase-like	Rattus norvegicus	93-97
25041240-10	2014	These actions of AEA and 2-AG are tightly regulated by their respective degradative enzymes, FAAH and MGL.	aea	17-20	monoglyceride lipase	Rattus norvegicus	102-105
25568329-5	2015	We demonstrate that microglial extracellular vesicles carry on their surface N-arachidonoylethanolamine (AEA), which is able to stimulate type-1 cannabinoid receptors (CB1), and inhibit presynaptic transmission, in target GABAergic neurons.	aea	77-103	cannabinoid receptor 1	Homo sapiens	168-171
25568329-5	2015	We demonstrate that microglial extracellular vesicles carry on their surface N-arachidonoylethanolamine (AEA), which is able to stimulate type-1 cannabinoid receptors (CB1), and inhibit presynaptic transmission, in target GABAergic neurons.	aea	105-108	cannabinoid receptor 1	Homo sapiens	168-171
24998969-3	2014	FNT oxon (bioactive metabolite of FNT) preferentially inhibited the fatty acid amide hydrolase (FAAH), an endocannabinoid anandamide (AEA) hydrolase, in the rat cellular membrane preparation from the testis in vitro.	aea	134-137	fatty-acid amide hydrolase-like	Rattus norvegicus	96-100
24998969-6	2014	Intriguingly, testicular AEA (endogenous substrate of FAAH) levels were elevated along with the FAAH inhibition caused by the subchronic exposure.	aea	25-28	fatty-acid amide hydrolase-like	Rattus norvegicus	54-58
25003845-2	2014	The best-known mammalian compound of this class is anandamide, N-arachidonoylethanolamine, one of the endogenous ligands of cannabinoid CB1 and CB2 receptors.	aea	63-89	cannabinoid receptor 1	Homo sapiens	136-139
25003845-2	2014	The best-known mammalian compound of this class is anandamide, N-arachidonoylethanolamine, one of the endogenous ligands of cannabinoid CB1 and CB2 receptors.	aea	63-89	cannabinoid receptor 2	Homo sapiens	144-147
24998969-6	2014	Intriguingly, testicular AEA (endogenous substrate of FAAH) levels were elevated along with the FAAH inhibition caused by the subchronic exposure.	aea	25-28	fatty-acid amide hydrolase-like	Rattus norvegicus	96-100
24849924-1	2014	Complementary genetic and pharmacological approaches to inhibit monoacylglycerol lipase (MAGL) and fatty acid amide hydrolase (FAAH), the primary hydrolytic enzymes of the respective endogenous cannabinoids 2-arachidonoylglycerol (2-AG) and N-arachidonoylethanolamine, enable the exploration of potential therapeutic applications and physiologic roles of these enzymes.	aea	241-267	monoglyceride lipase	Mus musculus	64-87
25058512-2	2014	However, recent preclinical data indicate that combined inhibition of cyclooxygenase (COX) and fatty acid amide hydrolase (FAAH), the primary catabolic enzyme of the endocannabinoid N-arachidonoylethanolamine (anandamide; AEA), produces enhanced antinociceptive effects in a variety of murine models of pain.	aea	182-208	fatty acid amide hydrolase	Mus musculus	106-121
25058512-2	2014	However, recent preclinical data indicate that combined inhibition of cyclooxygenase (COX) and fatty acid amide hydrolase (FAAH), the primary catabolic enzyme of the endocannabinoid N-arachidonoylethanolamine (anandamide; AEA), produces enhanced antinociceptive effects in a variety of murine models of pain.	aea	182-208	fatty acid amide hydrolase	Mus musculus	123-127
24849924-1	2014	Complementary genetic and pharmacological approaches to inhibit monoacylglycerol lipase (MAGL) and fatty acid amide hydrolase (FAAH), the primary hydrolytic enzymes of the respective endogenous cannabinoids 2-arachidonoylglycerol (2-AG) and N-arachidonoylethanolamine, enable the exploration of potential therapeutic applications and physiologic roles of these enzymes.	aea	241-267	monoglyceride lipase	Mus musculus	89-93
24849924-1	2014	Complementary genetic and pharmacological approaches to inhibit monoacylglycerol lipase (MAGL) and fatty acid amide hydrolase (FAAH), the primary hydrolytic enzymes of the respective endogenous cannabinoids 2-arachidonoylglycerol (2-AG) and N-arachidonoylethanolamine, enable the exploration of potential therapeutic applications and physiologic roles of these enzymes.	aea	241-267	fatty acid amide hydrolase	Mus musculus	110-125
24849924-1	2014	Complementary genetic and pharmacological approaches to inhibit monoacylglycerol lipase (MAGL) and fatty acid amide hydrolase (FAAH), the primary hydrolytic enzymes of the respective endogenous cannabinoids 2-arachidonoylglycerol (2-AG) and N-arachidonoylethanolamine, enable the exploration of potential therapeutic applications and physiologic roles of these enzymes.	aea	241-267	fatty acid amide hydrolase	Mus musculus	127-131
24510313-11	2014	We conclude that SCP-2 is a low affinity binding protein for AEA that can facilitate its cellular uptake but does not contribute significantly to intracellular sequestration of AEA.	aea	61-64	sterol carrier protein 2	Homo sapiens	17-22
24684963-3	2014	One lesser-known property of COX-2 is its ability to metabolize the endocannabinoids, N-arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol (2-AG).	aea	86-112	prostaglandin-endoperoxide synthase 2	Homo sapiens	29-34
24510313-6	2014	The docking studies predict that AEA and AM404 associate with SCP-2 at a putative cholesterol binding pocket with  G values of -3.6 and -4.6 kcal/mol, respectively.	aea	33-36	sterol carrier protein 2	Homo sapiens	62-67
24510313-8	2014	In support of the docking studies, SCP-2-mediated transfer of cholesterol in vitro is inhibited by micromolar concentrations of AEA; and heterologous expression of SCP-2 in HEK 293 cells increases time-related accumulation of AEA in a temperature-dependent fashion.	aea	128-131	sterol carrier protein 2	Homo sapiens	35-40
24510313-8	2014	In support of the docking studies, SCP-2-mediated transfer of cholesterol in vitro is inhibited by micromolar concentrations of AEA; and heterologous expression of SCP-2 in HEK 293 cells increases time-related accumulation of AEA in a temperature-dependent fashion.	aea	226-229	sterol carrier protein 2	Homo sapiens	35-40
24510313-8	2014	In support of the docking studies, SCP-2-mediated transfer of cholesterol in vitro is inhibited by micromolar concentrations of AEA; and heterologous expression of SCP-2 in HEK 293 cells increases time-related accumulation of AEA in a temperature-dependent fashion.	aea	226-229	sterol carrier protein 2	Homo sapiens	164-169
24510313-9	2014	These results suggest that SCP-2 facilitates cellular uptake of AEA.	aea	64-67	sterol carrier protein 2	Homo sapiens	27-32
24684963-3	2014	One lesser-known property of COX-2 is its ability to metabolize the endocannabinoids, N-arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol (2-AG).	aea	114-117	prostaglandin-endoperoxide synthase 2	Homo sapiens	29-34
24494681-2	2014	Increasing tissue levels of the CB1 receptor endogenous ligand N-arachidonoylethanolamine (anandamide), by inhibiting anandamide degradation through blocking the anandamide-hydrolysing enzyme fatty acid amide hydrolase, has been suggested to be used to activate the CB1 receptor.	aea	63-89	cannabinoid receptor 1	Homo sapiens	32-35
24531463-2	2014	To understand how the endocannabinoids bind to FABPs, the crystal structures of FABP5 in complex with AEA, 2-AG and the inhibitor BMS-309403 were determined.	aea	102-105	fatty acid binding protein 5	Homo sapiens	80-85
24494681-2	2014	Increasing tissue levels of the CB1 receptor endogenous ligand N-arachidonoylethanolamine (anandamide), by inhibiting anandamide degradation through blocking the anandamide-hydrolysing enzyme fatty acid amide hydrolase, has been suggested to be used to activate the CB1 receptor.	aea	63-89	cannabinoid receptor 1	Homo sapiens	266-269
24148808-5	2014	Peripheral subcutaneous injections of AEA, 2-AG, WIN55,212-2 (WIN; a CB1/CB2 synthetic agonist), URB597 and URB602 significantly decreased mechanical allodynia and thermal hyperalgesia.	aea	38-41	cannabinoid receptor 2 (macrophage)	Mus musculus	73-76
24148808-1	2014	The two most studied endocannabinoids are anandamide (AEA), principally catalyzed by fatty-acid amide hydrolase (FAAH), and 2-arachidonoyl glycerol (2-AG), mainly hydrolyzed by monoacylglycerol lipase (MGL).	aea	54-57	fatty acid amide hydrolase	Mus musculus	85-111
24148808-9	2014	The antinociceptive properties of AEA and URB597 were mediated only by CB1 receptors.	aea	34-37	cannabinoid receptor 1 (brain)	Mus musculus	71-74
24148808-1	2014	The two most studied endocannabinoids are anandamide (AEA), principally catalyzed by fatty-acid amide hydrolase (FAAH), and 2-arachidonoyl glycerol (2-AG), mainly hydrolyzed by monoacylglycerol lipase (MGL).	aea	54-57	fatty acid amide hydrolase	Mus musculus	113-117
24148808-3	2014	Several recent studies examining the contribution of CB1 and/or CB2 receptors on the peripheral antinociceptive effects of AEA, 2-AG, URB597 and URB602 in neuropathic pain conditions using either pharmacological tools or transgenic mice separately have been reported, but the exact mechanism is still uncertain.	aea	123-126	cannabinoid receptor 2 (macrophage)	Mus musculus	64-67
23347118-4	2013	EXPERIMENTAL APPROACH: The aim of this study was to analyse the effects of AEA or FAAH inhibition by the URB597 inhibitor or FAAH/siRNA on the activation of Nrf2-ARE signalling pathway and heme oxygenase-1 (HO-1) induction and transcription.	aea	75-78	NFE2 like bZIP transcription factor 2	Homo sapiens	157-161
24148808-5	2014	Peripheral subcutaneous injections of AEA, 2-AG, WIN55,212-2 (WIN; a CB1/CB2 synthetic agonist), URB597 and URB602 significantly decreased mechanical allodynia and thermal hyperalgesia.	aea	38-41	cannabinoid receptor 1 (brain)	Mus musculus	69-72
23347118-3	2013	Here, we investigated whether FAAH or AEA are involved in NF (erythroid-derived 2)-like 2 (Nrf2)/antioxidant responsive element (ARE) pathway.	aea	38-41	NFE2 like bZIP transcription factor 2	Homo sapiens	91-95
23347118-4	2013	EXPERIMENTAL APPROACH: The aim of this study was to analyse the effects of AEA or FAAH inhibition by the URB597 inhibitor or FAAH/siRNA on the activation of Nrf2-ARE signalling pathway and heme oxygenase-1 (HO-1) induction and transcription.	aea	75-78	heme oxygenase 1	Homo sapiens	189-205
23347118-4	2013	EXPERIMENTAL APPROACH: The aim of this study was to analyse the effects of AEA or FAAH inhibition by the URB597 inhibitor or FAAH/siRNA on the activation of Nrf2-ARE signalling pathway and heme oxygenase-1 (HO-1) induction and transcription.	aea	75-78	heme oxygenase 1	Homo sapiens	207-211
23347118-9	2013	Furthermore, URB597, AEA and siRNA-FAAH treatments induced the nuclear translocation of Nrf2, while siRNA-Nrf2 treatment and Keap1 expression blocked AEA, URB597 and si-FAAH from activation of ARE reporter and HO-1 induction.	aea	21-24	NFE2 like bZIP transcription factor 2	Homo sapiens	88-92
23347118-9	2013	Furthermore, URB597, AEA and siRNA-FAAH treatments induced the nuclear translocation of Nrf2, while siRNA-Nrf2 treatment and Keap1 expression blocked AEA, URB597 and si-FAAH from activation of ARE reporter and HO-1 induction.	aea	21-24	kelch like ECH associated protein 1	Homo sapiens	125-130
23347118-9	2013	Furthermore, URB597, AEA and siRNA-FAAH treatments induced the nuclear translocation of Nrf2, while siRNA-Nrf2 treatment and Keap1 expression blocked AEA, URB597 and si-FAAH from activation of ARE reporter and HO-1 induction.	aea	21-24	fatty acid amide hydrolase	Homo sapiens	169-173
23347118-9	2013	Furthermore, URB597, AEA and siRNA-FAAH treatments induced the nuclear translocation of Nrf2, while siRNA-Nrf2 treatment and Keap1 expression blocked AEA, URB597 and si-FAAH from activation of ARE reporter and HO-1 induction.	aea	150-153	fatty acid amide hydrolase	Homo sapiens	35-39
23347118-9	2013	Furthermore, URB597, AEA and siRNA-FAAH treatments induced the nuclear translocation of Nrf2, while siRNA-Nrf2 treatment and Keap1 expression blocked AEA, URB597 and si-FAAH from activation of ARE reporter and HO-1 induction.	aea	150-153	NFE2 like bZIP transcription factor 2	Homo sapiens	88-92
23347118-9	2013	Furthermore, URB597, AEA and siRNA-FAAH treatments induced the nuclear translocation of Nrf2, while siRNA-Nrf2 treatment and Keap1 expression blocked AEA, URB597 and si-FAAH from activation of ARE reporter and HO-1 induction.	aea	150-153	NFE2 like bZIP transcription factor 2	Homo sapiens	106-110
23347118-9	2013	Furthermore, URB597, AEA and siRNA-FAAH treatments induced the nuclear translocation of Nrf2, while siRNA-Nrf2 treatment and Keap1 expression blocked AEA, URB597 and si-FAAH from activation of ARE reporter and HO-1 induction.	aea	150-153	kelch like ECH associated protein 1	Homo sapiens	125-130
23347118-9	2013	Furthermore, URB597, AEA and siRNA-FAAH treatments induced the nuclear translocation of Nrf2, while siRNA-Nrf2 treatment and Keap1 expression blocked AEA, URB597 and si-FAAH from activation of ARE reporter and HO-1 induction.	aea	150-153	heme oxygenase 1	Homo sapiens	210-214
23347118-11	2013	CONCLUSIONS AND IMPLICATIONS: These data uncovered a novel mechanism by which inhibition of FAAH or exposure to AEA induced HO-1 transcripts and implicating AEA and FAAH as direct modifiers in signalling mediated activation of Nrf2-HO-1 pathway, independent of cannabinoid receptors.	aea	112-115	heme oxygenase 1	Homo sapiens	124-128
23347118-11	2013	CONCLUSIONS AND IMPLICATIONS: These data uncovered a novel mechanism by which inhibition of FAAH or exposure to AEA induced HO-1 transcripts and implicating AEA and FAAH as direct modifiers in signalling mediated activation of Nrf2-HO-1 pathway, independent of cannabinoid receptors.	aea	112-115	fatty acid amide hydrolase	Homo sapiens	165-169
23347118-11	2013	CONCLUSIONS AND IMPLICATIONS: These data uncovered a novel mechanism by which inhibition of FAAH or exposure to AEA induced HO-1 transcripts and implicating AEA and FAAH as direct modifiers in signalling mediated activation of Nrf2-HO-1 pathway, independent of cannabinoid receptors.	aea	112-115	NFE2 like bZIP transcription factor 2	Homo sapiens	227-231
23347118-11	2013	CONCLUSIONS AND IMPLICATIONS: These data uncovered a novel mechanism by which inhibition of FAAH or exposure to AEA induced HO-1 transcripts and implicating AEA and FAAH as direct modifiers in signalling mediated activation of Nrf2-HO-1 pathway, independent of cannabinoid receptors.	aea	112-115	heme oxygenase 1	Homo sapiens	232-236
23347118-11	2013	CONCLUSIONS AND IMPLICATIONS: These data uncovered a novel mechanism by which inhibition of FAAH or exposure to AEA induced HO-1 transcripts and implicating AEA and FAAH as direct modifiers in signalling mediated activation of Nrf2-HO-1 pathway, independent of cannabinoid receptors.	aea	157-160	fatty acid amide hydrolase	Homo sapiens	92-96
23347118-11	2013	CONCLUSIONS AND IMPLICATIONS: These data uncovered a novel mechanism by which inhibition of FAAH or exposure to AEA induced HO-1 transcripts and implicating AEA and FAAH as direct modifiers in signalling mediated activation of Nrf2-HO-1 pathway, independent of cannabinoid receptors.	aea	157-160	heme oxygenase 1	Homo sapiens	124-128
23347118-11	2013	CONCLUSIONS AND IMPLICATIONS: These data uncovered a novel mechanism by which inhibition of FAAH or exposure to AEA induced HO-1 transcripts and implicating AEA and FAAH as direct modifiers in signalling mediated activation of Nrf2-HO-1 pathway, independent of cannabinoid receptors.	aea	157-160	NFE2 like bZIP transcription factor 2	Homo sapiens	227-231
23347118-11	2013	CONCLUSIONS AND IMPLICATIONS: These data uncovered a novel mechanism by which inhibition of FAAH or exposure to AEA induced HO-1 transcripts and implicating AEA and FAAH as direct modifiers in signalling mediated activation of Nrf2-HO-1 pathway, independent of cannabinoid receptors.	aea	157-160	heme oxygenase 1	Homo sapiens	232-236
23643752-1	2013	The endocannabinoid, N-arachidonoylethanolamine (AEA), is degraded by the enzyme fatty acid amide hydrolase (FAAH).	aea	21-47	fatty-acid amide hydrolase-like	Rattus norvegicus	81-107
23643752-1	2013	The endocannabinoid, N-arachidonoylethanolamine (AEA), is degraded by the enzyme fatty acid amide hydrolase (FAAH).	aea	21-47	fatty-acid amide hydrolase-like	Rattus norvegicus	109-113
23643752-1	2013	The endocannabinoid, N-arachidonoylethanolamine (AEA), is degraded by the enzyme fatty acid amide hydrolase (FAAH).	aea	49-52	fatty-acid amide hydrolase-like	Rattus norvegicus	81-107
23643752-1	2013	The endocannabinoid, N-arachidonoylethanolamine (AEA), is degraded by the enzyme fatty acid amide hydrolase (FAAH).	aea	49-52	fatty-acid amide hydrolase-like	Rattus norvegicus	109-113
23488865-1	2013	INTRODUCTION: Fatty acid amide hydrolase (FAAH) is the major catabolic enzyme of the endocannabinoid N-arachidonoylethanolamine (anandamide) that, with different degrees of efficiency, also hydrolyzes other endogenous fatty acid ethanolamides.	aea	101-127	fatty acid amide hydrolase	Homo sapiens	14-40
23563893-9	2013	Taken together, these findings indicate that AEA-mediated activation of CB1 receptors is crucial for social interaction, and that PCP-induced social withdrawal results from deficient endocannabinoid transmission.	aea	45-48	cannabinoid receptor 1	Rattus norvegicus	72-75
23307660-6	2013	The degradation enzyme of 2-arachidonoylglycerol (2-AG), monoacylglycerol lipase, blocked DSE, while another catabolism enzyme for N-arachidonoylethanolamine, fatty acid amide hydrolase, did not, suggesting that 2-AG is responsible for DSE in Purkinje cells.	aea	131-157	monoglyceride lipase	Mus musculus	57-80
23488865-1	2013	INTRODUCTION: Fatty acid amide hydrolase (FAAH) is the major catabolic enzyme of the endocannabinoid N-arachidonoylethanolamine (anandamide) that, with different degrees of efficiency, also hydrolyzes other endogenous fatty acid ethanolamides.	aea	101-127	fatty acid amide hydrolase	Homo sapiens	42-46
23512546-2	2013	The principal ligands of the endocannabinoid system are the lipid transmitters N-arachidonoylethanolamine (anandamide) and 2-arachidonoylglycerol (2-AG), which activate the two major cannabinoid receptors, CB1 and CB2.	aea	79-105	cannabinoid receptor 1	Homo sapiens	206-209
23183551-2	2013	Whereas lower doses of AEA induce anxiolytic-like effects by activating cannabinoid CB1 receptors, no effects are observed with higher doses, possibly due to the simultaneous activation of transient receptor potential vanilloid type 1 (TRPV1) receptors.	aea	23-26	cannabinoid receptor 1	Rattus norvegicus	84-87
23183551-2	2013	Whereas lower doses of AEA induce anxiolytic-like effects by activating cannabinoid CB1 receptors, no effects are observed with higher doses, possibly due to the simultaneous activation of transient receptor potential vanilloid type 1 (TRPV1) receptors.	aea	23-26	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	189-234
23183551-2	2013	Whereas lower doses of AEA induce anxiolytic-like effects by activating cannabinoid CB1 receptors, no effects are observed with higher doses, possibly due to the simultaneous activation of transient receptor potential vanilloid type 1 (TRPV1) receptors.	aea	23-26	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	236-241
23183551-4	2013	OBJECTIVE: Considering that the blockade of TRPV1 or NMDA receptors in the dlPAG induces anxiolytic-like effects, we tested the hypothesis that facilitation of glutamate transmission through TRPV1 is responsible for the lack of anxiolytic-like effect observed with high AEA doses.	aea	270-273	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	191-196
23512546-2	2013	The principal ligands of the endocannabinoid system are the lipid transmitters N-arachidonoylethanolamine (anandamide) and 2-arachidonoylglycerol (2-AG), which activate the two major cannabinoid receptors, CB1 and CB2.	aea	79-105	cannabinoid receptor 2	Homo sapiens	214-217
22891244-4	2012	In this study the influence of the endocannabinoids, anandamide (AEA) and 2-arachidonoylglycerol, on the Notch-1 pathway and on its endogenous regulators were investigated in an in vitro model of AD.	aea	65-68	notch receptor 1	Rattus norvegicus	105-112
23169348-11	2013	Both CB(1) (by AEA and 2-AG) and non-CB(1) (by OEA) targets can alter the excitability and activity of the dopaminergic neurons in the VTA.	aea	15-18	cannabinoid receptor 1	Homo sapiens	5-10
22947916-6	2013	Endocannabinoids such as anandamide [N-arachidonoylethanolamine (AEA)] and 2-arachidonoyl glycerol (2-AG) are known as orexigenic mediators that act via cannabinoid receptor 1 (CB1) in the hypothalamus and limbic forebrain to induce appetite and stimulate food intake.	aea	37-63	cannabinoid receptor 1	Homo sapiens	153-175
22947916-6	2013	Endocannabinoids such as anandamide [N-arachidonoylethanolamine (AEA)] and 2-arachidonoyl glycerol (2-AG) are known as orexigenic mediators that act via cannabinoid receptor 1 (CB1) in the hypothalamus and limbic forebrain to induce appetite and stimulate food intake.	aea	37-63	cannabinoid receptor 1	Homo sapiens	177-180
22947916-6	2013	Endocannabinoids such as anandamide [N-arachidonoylethanolamine (AEA)] and 2-arachidonoyl glycerol (2-AG) are known as orexigenic mediators that act via cannabinoid receptor 1 (CB1) in the hypothalamus and limbic forebrain to induce appetite and stimulate food intake.	aea	65-68	cannabinoid receptor 1	Homo sapiens	153-175
22947916-6	2013	Endocannabinoids such as anandamide [N-arachidonoylethanolamine (AEA)] and 2-arachidonoyl glycerol (2-AG) are known as orexigenic mediators that act via cannabinoid receptor 1 (CB1) in the hypothalamus and limbic forebrain to induce appetite and stimulate food intake.	aea	65-68	cannabinoid receptor 1	Homo sapiens	177-180
22891244-5	2012	We report that AEA up-regulates Notch-1 signaling in cultured neurons.	aea	15-18	notch receptor 1	Rattus norvegicus	32-39
22891244-6	2012	We also provide evidence that although Abeta(1-42) increases expression of the endogenous inhibitor of Notch-1, numb (Nb), this can be prevented by AEA and 2-arachidonoylglycerol.	aea	148-151	notch receptor 1	Rattus norvegicus	103-110
22891244-6	2012	We also provide evidence that although Abeta(1-42) increases expression of the endogenous inhibitor of Notch-1, numb (Nb), this can be prevented by AEA and 2-arachidonoylglycerol.	aea	148-151	NUMB, endocytic adaptor protein	Rattus norvegicus	112-116
22891244-6	2012	We also provide evidence that although Abeta(1-42) increases expression of the endogenous inhibitor of Notch-1, numb (Nb), this can be prevented by AEA and 2-arachidonoylglycerol.	aea	148-151	NUMB, endocytic adaptor protein	Rattus norvegicus	118-120
22891244-7	2012	Interestingly, AEA up-regulated Nct expression, a component of gamma-secretase, and this was found to play a crucial role in the enhanced Notch-1 signaling mediated by AEA.	aea	15-18	notch receptor 1	Rattus norvegicus	138-145
22891244-7	2012	Interestingly, AEA up-regulated Nct expression, a component of gamma-secretase, and this was found to play a crucial role in the enhanced Notch-1 signaling mediated by AEA.	aea	168-171	notch receptor 1	Rattus norvegicus	138-145
22891244-8	2012	The stimulatory effects of AEA on Notch-1 signaling persisted in the presence of Abeta(1-42).	aea	27-30	notch receptor 1	Rattus norvegicus	34-41
22891244-9	2012	AEA was found to induce a preferential processing of Notch-1 over amyloid precursor protein to generate Abeta(1-40).	aea	0-3	notch receptor 1	Rattus norvegicus	53-60
22891244-9	2012	AEA was found to induce a preferential processing of Notch-1 over amyloid precursor protein to generate Abeta(1-40).	aea	0-3	amyloid beta precursor protein	Rattus norvegicus	66-91
22891244-11	2012	In summary, AEA has the proclivity to enhance Notch-1 signaling in an in vitro model of AD, which may have relevance for restoring neurogenesis and cognition in AD.	aea	12-15	notch receptor 1	Rattus norvegicus	46-53
22593077-7	2012	Intraplantar injection of AEA (10 mug/10 mul) or URB597 (9 mug/10 mul) transiently attenuated hyperalgesia through activation of peripheral CB1 receptors.	aea	26-29	cannabinoid receptor 1	Homo sapiens	140-143
22514334-2	2012	Brain enzymatic activity of FAAH and the endogenous levels of its substrates, anandamide (AEA; N-arachidonoylethanolamine), 2-arachidonoylglycerol (2-AG), and N-palmitoylethanolamine (PEA), were measured in control and ST4070-treated mice.	aea	95-121	fatty acid amide hydrolase	Mus musculus	28-32
21844878-10	2012	CONCLUSION: These findings suggest that AEA might be a physiological meal initiator in humans and furthermore show that postprandially AEA and PYY are concomitantly deregulated in obesity.	aea	40-43	peptide YY	Homo sapiens	143-146
22595113-5	2012	METHODS: We examined AEA-induced MMP-2 production and the expression of AEA receptors (cannabinoid [CB] receptor-1, CB2, and transient receptor potential vanilloid-1 [TRPV1]) in HPC by Western blot.	aea	21-24	matrix metallopeptidase 2	Homo sapiens	33-38
22595113-8	2012	RESULTS: AEA significantly induced MMP-2 production in HPC.	aea	9-12	matrix metallopeptidase 2	Homo sapiens	35-40
22595113-10	2012	AEA-induced MMP-2 production was blocked by CB1 or TRPV1 antagonists and by small interfering RNA for CB1 or TRPV1.	aea	0-3	matrix metallopeptidase 2	Homo sapiens	12-17
22595113-10	2012	AEA-induced MMP-2 production was blocked by CB1 or TRPV1 antagonists and by small interfering RNA for CB1 or TRPV1.	aea	0-3	cannabinoid receptor 1	Homo sapiens	44-47
22595113-10	2012	AEA-induced MMP-2 production was blocked by CB1 or TRPV1 antagonists and by small interfering RNA for CB1 or TRPV1.	aea	0-3	transient receptor potential cation channel subfamily V member 1	Homo sapiens	51-56
22595113-10	2012	AEA-induced MMP-2 production was blocked by CB1 or TRPV1 antagonists and by small interfering RNA for CB1 or TRPV1.	aea	0-3	cannabinoid receptor 1	Homo sapiens	102-105
22595113-10	2012	AEA-induced MMP-2 production was blocked by CB1 or TRPV1 antagonists and by small interfering RNA for CB1 or TRPV1.	aea	0-3	transient receptor potential cation channel subfamily V member 1	Homo sapiens	109-114
22595113-12	2012	CONCLUSIONS: We demonstrated for the first time that AEA induced MMP-2 production via CB1 and TRPV1 in HPC.	aea	53-56	matrix metallopeptidase 2	Homo sapiens	65-70
22595113-12	2012	CONCLUSIONS: We demonstrated for the first time that AEA induced MMP-2 production via CB1 and TRPV1 in HPC.	aea	53-56	cannabinoid receptor 1	Homo sapiens	86-89
22595113-12	2012	CONCLUSIONS: We demonstrated for the first time that AEA induced MMP-2 production via CB1 and TRPV1 in HPC.	aea	53-56	transient receptor potential cation channel subfamily V member 1	Homo sapiens	94-99
22860206-1	2012	Fatty acid amide hydrolase (FAAH) plays the central role in the degradation of bioactive N-acylethanolamines such as the endocannabinoid arachidonoylethanolamide (anandamide) in brain and peripheral tissues.	aea	163-173	fatty acid amide hydrolase	Mus musculus	11-26
22860206-1	2012	Fatty acid amide hydrolase (FAAH) plays the central role in the degradation of bioactive N-acylethanolamines such as the endocannabinoid arachidonoylethanolamide (anandamide) in brain and peripheral tissues.	aea	163-173	fatty acid amide hydrolase	Mus musculus	28-32
22850591-1	2012	The endocannabinoid anandamide (N-arachidonoylethanolamine, AEA), a physiologically occurring bioactive compound on CB1 and CB2 receptors, has multiple physiological functions.	aea	32-58	cannabinoid receptor 1	Homo sapiens	116-119
22850591-1	2012	The endocannabinoid anandamide (N-arachidonoylethanolamine, AEA), a physiologically occurring bioactive compound on CB1 and CB2 receptors, has multiple physiological functions.	aea	32-58	cannabinoid receptor 2	Homo sapiens	124-127
22850591-1	2012	The endocannabinoid anandamide (N-arachidonoylethanolamine, AEA), a physiologically occurring bioactive compound on CB1 and CB2 receptors, has multiple physiological functions.	aea	60-63	cannabinoid receptor 1	Homo sapiens	116-119
22850591-1	2012	The endocannabinoid anandamide (N-arachidonoylethanolamine, AEA), a physiologically occurring bioactive compound on CB1 and CB2 receptors, has multiple physiological functions.	aea	60-63	cannabinoid receptor 2	Homo sapiens	124-127
22447182-4	2012	Further, the studied human melanoma cell lines expressed functional CB1 since physiological and synthetic ligands, anandamide (AEA), Met-F-AEA, ACEA and AM251 showed a wide range of biological effects in vitro, for example anti-proliferative, proapoptotic and anti-migratory.	aea	127-130	cannabinoid receptor 1	Homo sapiens	68-71
22860205-2	2012	N-Arachidonoylethanolamine (anandamide; AEA) and 2-arachidonoylglycerol (2-AG) are endogenous cannabinoids that are predominantly metabolized by the respective enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL).	aea	0-26	fatty acid amide hydrolase	Mus musculus	179-194
22860205-2	2012	N-Arachidonoylethanolamine (anandamide; AEA) and 2-arachidonoylglycerol (2-AG) are endogenous cannabinoids that are predominantly metabolized by the respective enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL).	aea	0-26	fatty acid amide hydrolase	Mus musculus	196-200
22860205-2	2012	N-Arachidonoylethanolamine (anandamide; AEA) and 2-arachidonoylglycerol (2-AG) are endogenous cannabinoids that are predominantly metabolized by the respective enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL).	aea	0-26	monoglyceride lipase	Mus musculus	206-229
22860205-2	2012	N-Arachidonoylethanolamine (anandamide; AEA) and 2-arachidonoylglycerol (2-AG) are endogenous cannabinoids that are predominantly metabolized by the respective enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL).	aea	0-26	monoglyceride lipase	Mus musculus	231-235
22371393-6	2012	Analysis of a panel of subinterval congenic mice showed that the full effect of Lbw2 on AEA production was dependent on three subloci, with splenomegaly mapping to two of the subloci and expansions of peritoneal cell populations, including B-1a cells to one.	aea	88-91	lupus NZB x NZW 2	Mus musculus	80-84
21185816-5	2011	These simulations are compared with a 70 ns simulation of the cannabinoid CB1 receptor endogenous ligand, N-arachidonoylethanolamine (anandamide, AEA) in a POPC bilayer.	aea	106-132	cannabinoid receptor 1	Homo sapiens	74-77
22107886-1	2012	Fatty acid amide hydrolase (FAAH) is one of the main enzymes responsible for the degradation of the endocannabinoid anandamide (N-arachidonoylethanolamine, AEA).	aea	128-154	fatty-acid amide hydrolase-like	Rattus norvegicus	28-32
22927908-6	2012	The degradation enzyme of 2-arachidonoylglycerol (2-AG), monoacylglycerol lipase (MAGL), blocked DSE, while another catabolism enzyme for N-arachidonoylethanolamine (AEA), fatty acid amide hydrolase (FAAH), did not affect DSE.	aea	138-164	monoglyceride lipase	Mus musculus	57-80
22927908-6	2012	The degradation enzyme of 2-arachidonoylglycerol (2-AG), monoacylglycerol lipase (MAGL), blocked DSE, while another catabolism enzyme for N-arachidonoylethanolamine (AEA), fatty acid amide hydrolase (FAAH), did not affect DSE.	aea	138-164	monoglyceride lipase	Mus musculus	82-86
22927908-6	2012	The degradation enzyme of 2-arachidonoylglycerol (2-AG), monoacylglycerol lipase (MAGL), blocked DSE, while another catabolism enzyme for N-arachidonoylethanolamine (AEA), fatty acid amide hydrolase (FAAH), did not affect DSE.	aea	138-164	fatty acid amide hydrolase	Mus musculus	183-198
22927908-6	2012	The degradation enzyme of 2-arachidonoylglycerol (2-AG), monoacylglycerol lipase (MAGL), blocked DSE, while another catabolism enzyme for N-arachidonoylethanolamine (AEA), fatty acid amide hydrolase (FAAH), did not affect DSE.	aea	138-164	fatty acid amide hydrolase	Mus musculus	200-204
22927908-6	2012	The degradation enzyme of 2-arachidonoylglycerol (2-AG), monoacylglycerol lipase (MAGL), blocked DSE, while another catabolism enzyme for N-arachidonoylethanolamine (AEA), fatty acid amide hydrolase (FAAH), did not affect DSE.	aea	166-169	monoglyceride lipase	Mus musculus	57-80
22927908-6	2012	The degradation enzyme of 2-arachidonoylglycerol (2-AG), monoacylglycerol lipase (MAGL), blocked DSE, while another catabolism enzyme for N-arachidonoylethanolamine (AEA), fatty acid amide hydrolase (FAAH), did not affect DSE.	aea	166-169	monoglyceride lipase	Mus musculus	82-86
22927908-6	2012	The degradation enzyme of 2-arachidonoylglycerol (2-AG), monoacylglycerol lipase (MAGL), blocked DSE, while another catabolism enzyme for N-arachidonoylethanolamine (AEA), fatty acid amide hydrolase (FAAH), did not affect DSE.	aea	166-169	fatty acid amide hydrolase	Mus musculus	183-198
22927908-6	2012	The degradation enzyme of 2-arachidonoylglycerol (2-AG), monoacylglycerol lipase (MAGL), blocked DSE, while another catabolism enzyme for N-arachidonoylethanolamine (AEA), fatty acid amide hydrolase (FAAH), did not affect DSE.	aea	166-169	fatty acid amide hydrolase	Mus musculus	200-204
21924613-3	2011	Fatty acid amide hydrolase (FAAH) is an integral membrane serine hydrolase responsible for the degradation of fatty acid amide signaling molecules such as endocannabinoid anandamide (AEA), which has been shown to possess cannabinoid-like analgesic properties.	aea	183-186	fatty acid amide hydrolase	Homo sapiens	0-26
21924613-3	2011	Fatty acid amide hydrolase (FAAH) is an integral membrane serine hydrolase responsible for the degradation of fatty acid amide signaling molecules such as endocannabinoid anandamide (AEA), which has been shown to possess cannabinoid-like analgesic properties.	aea	183-186	fatty acid amide hydrolase	Homo sapiens	28-32
21562266-1	2011	Two endogenous ligands for cannabinoid CB1 receptors, anandamide (N-arachidonoylethanolamine) and 2-arachidonoylglycerol (2-AG), have been identified and characterized.	aea	66-92	cannabinoid receptor 1	Homo sapiens	39-42
21331757-5	2011	In addition, the effect of AEA (administered 30 min before NTG injection) was investigated on NTG-induced Fos expression and evaluated 4 h following NTG injection.	aea	27-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
21331757-7	2011	Pre-treatment with AEA significantly reduced the NTG-induced neuronal activation in nucleus trigeminalis caudalis, confirming the results obtained in our previous study, and in area postrema, while the same treatment induced an increase of Fos expression in paraventricular and supraoptic nuclei of the hypothalamus, parabrachial nucleus, and periaqueductal grey.	aea	19-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	240-243
21987372-4	2012	CB1R messenger RNA expression was strongly decreased by SR141716, whereas it was increased by the CB1R agonist, arachidonic acid N-hydroxyethylamide (AEA), indicating the effectiveness of treatments in modulating ECS activity in liver explants both from lean or ob/ob mice.	aea	150-153	cannabinoid receptor 1 (brain)	Mus musculus	98-102
21987372-6	2012	In line with this, SR141716 stimulated ss-oxidation activity, and the role of CB1R in regulating this pathway was particularly emphasized when ECS was hyperactivated by AEA and in ob/ob tissue.	aea	169-172	cannabinoid receptor 1 (brain)	Mus musculus	78-82
22087025-1	2012	The cannabinoid receptor type 1 (CB1) is a G protein-coupled receptor that is activated in an autocrine fashion by the endocannabinoids (EC), N-arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol (2-AG).	aea	142-168	cannabinoid receptor 1	Homo sapiens	4-36
22087025-1	2012	The cannabinoid receptor type 1 (CB1) is a G protein-coupled receptor that is activated in an autocrine fashion by the endocannabinoids (EC), N-arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol (2-AG).	aea	170-173	cannabinoid receptor 1	Homo sapiens	4-36
22087025-9	2012	Consistent with this possibility, RhoA activity is significantly diminished by the exogenous application of AEA but not by 2-AG in PC-3 cells (cells with very low AEA hydrolysis).	aea	108-111	ras homolog family member A	Homo sapiens	34-38
22087025-9	2012	Consistent with this possibility, RhoA activity is significantly diminished by the exogenous application of AEA but not by 2-AG in PC-3 cells (cells with very low AEA hydrolysis).	aea	163-166	ras homolog family member A	Homo sapiens	34-38
21719468-3	2011	The endogenous cannabinoids, N-arachidonoylethanolamine (anandamide; AEA) and 2-arachidonylglycerol (2-AG), activate both cannabinoid receptors but are rapidly metabolized by fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL), respectively.	aea	29-55	fatty acid amide hydrolase	Mus musculus	186-201
21719468-3	2011	The endogenous cannabinoids, N-arachidonoylethanolamine (anandamide; AEA) and 2-arachidonylglycerol (2-AG), activate both cannabinoid receptors but are rapidly metabolized by fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL), respectively.	aea	29-55	fatty acid amide hydrolase	Mus musculus	203-207
21719468-3	2011	The endogenous cannabinoids, N-arachidonoylethanolamine (anandamide; AEA) and 2-arachidonylglycerol (2-AG), activate both cannabinoid receptors but are rapidly metabolized by fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL), respectively.	aea	29-55	monoglyceride lipase	Mus musculus	213-236
21719468-3	2011	The endogenous cannabinoids, N-arachidonoylethanolamine (anandamide; AEA) and 2-arachidonylglycerol (2-AG), activate both cannabinoid receptors but are rapidly metabolized by fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL), respectively.	aea	29-55	monoglyceride lipase	Mus musculus	238-242
21740924-1	2011	Fatty acid amide hydrolase (FAAH) is the primary degradative enzyme of the endocannabinoid anandamide (N-arachidonoylethanolamine), which activates cannabinoid CB(1) and CB(2) receptors.	aea	103-129	fatty acid amide hydrolase	Mus musculus	11-26
21740924-1	2011	Fatty acid amide hydrolase (FAAH) is the primary degradative enzyme of the endocannabinoid anandamide (N-arachidonoylethanolamine), which activates cannabinoid CB(1) and CB(2) receptors.	aea	103-129	fatty acid amide hydrolase	Mus musculus	28-32
21272594-5	2011	Activation of apamin-sensitive, small conductance Ca(2+)-activated K(+) (SK) channels, probably SK2 and SK3 as the immunofluorescence analysis indicated, attributed largely to the AEA action on mAHP.	aea	180-183	potassium calcium-activated channel subfamily N member 2	Rattus norvegicus	96-99
21272594-5	2011	Activation of apamin-sensitive, small conductance Ca(2+)-activated K(+) (SK) channels, probably SK2 and SK3 as the immunofluorescence analysis indicated, attributed largely to the AEA action on mAHP.	aea	180-183	potassium calcium-activated channel subfamily N member 3	Rattus norvegicus	104-107
21272594-9	2011	Thus, AEA might enhance the SK mAHP currents mainly in a non-CB1/TRPV1 receptor way.	aea	6-9	cannabinoid receptor 1	Rattus norvegicus	61-64
21272594-9	2011	Thus, AEA might enhance the SK mAHP currents mainly in a non-CB1/TRPV1 receptor way.	aea	6-9	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	65-70
20702753-3	2010	Along with arachidonic acid, COX-2 oxygenates the endocannabinoids anandamide (AEA) and 2-arachidonoylglycerol in vitro.	aea	79-82	prostaglandin-endoperoxide synthase 2	Mus musculus	29-34
22027193-5	2011	Propofol (50 microM) significantly attenuated cell death induced by AEA, showing a protective effect against ROS production and caspase-3 activity.	aea	68-71	caspase 3	Homo sapiens	128-137
20702753-7	2010	Although AEA is hydrolyzed primarily by fatty acid amide hydrolase (FAAH), ex vivo autoradiography revealed that COX-2 inhibition by nimesulide redirected [(3)H]AEA substrate from COX-2 to FAAH in the cortex, hippocampus, thalamus, and periaqueductal gray.	aea	9-12	fatty acid amide hydrolase	Mus musculus	51-66
20702753-7	2010	Although AEA is hydrolyzed primarily by fatty acid amide hydrolase (FAAH), ex vivo autoradiography revealed that COX-2 inhibition by nimesulide redirected [(3)H]AEA substrate from COX-2 to FAAH in the cortex, hippocampus, thalamus, and periaqueductal gray.	aea	9-12	fatty acid amide hydrolase	Mus musculus	68-72
20702753-7	2010	Although AEA is hydrolyzed primarily by fatty acid amide hydrolase (FAAH), ex vivo autoradiography revealed that COX-2 inhibition by nimesulide redirected [(3)H]AEA substrate from COX-2 to FAAH in the cortex, hippocampus, thalamus, and periaqueductal gray.	aea	161-164	prostaglandin-endoperoxide synthase 2	Mus musculus	113-118
20702753-8	2010	These data indicate that COX-2 possesses the capacity to metabolize AEA in vivo and can compete with FAAH for AEA in several brain regions.	aea	68-71	prostaglandin-endoperoxide synthase 2	Mus musculus	25-30
20702753-8	2010	These data indicate that COX-2 possesses the capacity to metabolize AEA in vivo and can compete with FAAH for AEA in several brain regions.	aea	110-113	prostaglandin-endoperoxide synthase 2	Mus musculus	25-30
20702753-8	2010	These data indicate that COX-2 possesses the capacity to metabolize AEA in vivo and can compete with FAAH for AEA in several brain regions.	aea	110-113	fatty acid amide hydrolase	Mus musculus	101-105
20702753-12	2010	These temporal variations in COX-2 distribution reduced the enzyme"s contribution toward [(3)H]AEA metabolism in the somatosensory cortex at midnight.	aea	95-98	prostaglandin-endoperoxide synthase 2	Mus musculus	29-34
20375198-2	2010	Conversely, fatty acid amide hydrolase (FAAH), the chief catabolic enzyme regulating the endogenous cannabinoid N-arachidonoylethanolamine (anandamide), has emerged as an attractive target for treating pain and other conditions.	aea	112-138	fatty acid amide hydrolase	Mus musculus	23-38
20375198-2	2010	Conversely, fatty acid amide hydrolase (FAAH), the chief catabolic enzyme regulating the endogenous cannabinoid N-arachidonoylethanolamine (anandamide), has emerged as an attractive target for treating pain and other conditions.	aea	112-138	fatty acid amide hydrolase	Mus musculus	40-44
20590572-6	2010	The AEA- or HU210-induced cell death and MAPK activation were attenuated by CB(1) antagonists [SR141716 (rimonabant) and AM281], inhibitors of p38 and JNK-MAPKs or the antioxidant N-acetylcysteine.	aea	4-7	cannabinoid receptor 1	Homo sapiens	76-81
20357755-2	2010	However, the consequences of repeated administration of the endocannabinoid N-arachidonoyl ethanolamine (anandamide, AEA) on cannabinoid receptor regulation are unclear because of its rapid metabolism by fatty acid amide hydrolase (FAAH).	aea	76-103	fatty acid amide hydrolase	Mus musculus	215-230
20590572-6	2010	The AEA- or HU210-induced cell death and MAPK activation were attenuated by CB(1) antagonists [SR141716 (rimonabant) and AM281], inhibitors of p38 and JNK-MAPKs or the antioxidant N-acetylcysteine.	aea	4-7	mitogen-activated protein kinase 14	Homo sapiens	143-146
20029375-1	2010	RATIONALE: Fatty acid amide hydrolase (FAAH) is the main degrading enzyme of the fatty acid ethanolamides anandamide (AEA) and oleoylethanolamide (OEA), which have opposite effects on food intake and energy balance.	aea	118-121	fatty acid amide hydrolase	Mus musculus	11-37
20096328-2	2010	AEA is inactivated by fatty acid amide hydrolase (FAAH), that is inhibited competitively by hydroxyanandamides (HAEAs) generated from AEA by lipoxygenase activity.	aea	0-3	fatty acid amide hydrolase	Homo sapiens	50-54
20096328-2	2010	AEA is inactivated by fatty acid amide hydrolase (FAAH), that is inhibited competitively by hydroxyanandamides (HAEAs) generated from AEA by lipoxygenase activity.	aea	113-116	fatty acid amide hydrolase	Homo sapiens	50-54
19942623-6	2010	The DOX-induced MAPK activation and cell death were significantly enhanced when DOX was co-administered with CB1 agonists AEA or HU210.	aea	122-125	cannabinoid receptor 1	Homo sapiens	109-112
19942623-7	2010	Remarkably, cell death and MAPK activation induced by AEA, HU210, and DOX +/- AEA/HU210 were largely attenuated by either CB1 antagonists (rimonabant and AM281) or by inhibitors of p38 and JNK MAPKs.	aea	54-57	cannabinoid receptor 1	Homo sapiens	122-125
19942623-7	2010	Remarkably, cell death and MAPK activation induced by AEA, HU210, and DOX +/- AEA/HU210 were largely attenuated by either CB1 antagonists (rimonabant and AM281) or by inhibitors of p38 and JNK MAPKs.	aea	78-81	cannabinoid receptor 1	Homo sapiens	122-125
19942623-7	2010	Remarkably, cell death and MAPK activation induced by AEA, HU210, and DOX +/- AEA/HU210 were largely attenuated by either CB1 antagonists (rimonabant and AM281) or by inhibitors of p38 and JNK MAPKs.	aea	78-81	mitogen-activated protein kinase 14	Homo sapiens	181-184
19942623-7	2010	Remarkably, cell death and MAPK activation induced by AEA, HU210, and DOX +/- AEA/HU210 were largely attenuated by either CB1 antagonists (rimonabant and AM281) or by inhibitors of p38 and JNK MAPKs.	aea	78-81	mitogen-activated protein kinase 8	Homo sapiens	189-192
20029375-1	2010	RATIONALE: Fatty acid amide hydrolase (FAAH) is the main degrading enzyme of the fatty acid ethanolamides anandamide (AEA) and oleoylethanolamide (OEA), which have opposite effects on food intake and energy balance.	aea	118-121	fatty acid amide hydrolase	Mus musculus	39-43
20029375-9	2010	As expected, both AEA and OEA levels were increased in hypothalamus, small intestine and liver of FAAH(-/-) mice.	aea	18-21	fatty acid amide hydrolase	Mus musculus	98-102
20029375-10	2010	CONCLUSION: These results indicate that the lack of FAAH predominantly promotes energy storage by food intake-independent mechanisms, through the enhancement of AEA levels rather than promoting the anorexic effects of OEA.	aea	161-164	fatty acid amide hydrolase	Mus musculus	52-56
18329052-2	2008	N-arachidonoylethanolamine (anandamide, AEA), is a full agonist at both cannabinoid CB(1) receptors and "transient receptor potential vanilloid" type 1 (TRPV1) channels, and N-palmitoylethanolamine (PEA) potentiates these effects.	aea	0-26	transient receptor potential cation channel subfamily V member 1	Homo sapiens	104-151
20865375-2	2010	Recent studies demonstrated that sweet taste responses can be modulated by leptin and endocannabinoids [anandamide (N-arachidonoylethanolamine) and 2-arachidonoyl glycerol].	aea	116-142	leptin	Mus musculus	75-81
19666749-2	2009	N-Arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), two known eCBs, are degraded by fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL), respectively.	aea	0-26	fatty acid amide hydrolase	Mus musculus	111-126
19666749-2	2009	N-Arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), two known eCBs, are degraded by fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL), respectively.	aea	0-26	fatty acid amide hydrolase	Mus musculus	128-132
19666749-2	2009	N-Arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), two known eCBs, are degraded by fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL), respectively.	aea	0-26	monoglyceride lipase	Mus musculus	138-161
19666749-2	2009	N-Arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), two known eCBs, are degraded by fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL), respectively.	aea	0-26	monoglyceride lipase	Mus musculus	163-167
19666749-2	2009	N-Arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), two known eCBs, are degraded by fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL), respectively.	aea	28-31	fatty acid amide hydrolase	Mus musculus	111-126
19666749-2	2009	N-Arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), two known eCBs, are degraded by fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL), respectively.	aea	28-31	fatty acid amide hydrolase	Mus musculus	128-132
19666749-2	2009	N-Arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), two known eCBs, are degraded by fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL), respectively.	aea	28-31	monoglyceride lipase	Mus musculus	138-161
19666749-2	2009	N-Arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), two known eCBs, are degraded by fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL), respectively.	aea	28-31	monoglyceride lipase	Mus musculus	163-167
19285258-5	2009	The cannabinoid receptor type 1 (CB1), one of the two identified cannabinoid receptors, is expressed in energy-balance brain structures that are also able to readily produce or inactivate N-arachidonoyl ethanolamine (anandamide) and 2-arachidonoylglycerol (2AG), the most abundantly formed and released endocannabinoids.	aea	188-215	cannabinoid receptor 1	Homo sapiens	33-36
19647115-4	2009	Recently, we have shown that treatment of mouse primary Sertoli cells with FSH enhances the activity of the AEA hydrolase (fatty acid amide hydrolase, FAAH), whereas it does not affect the enzymes that synthesize AEA, nor the level of the AEA-binding type-2 cannabinoid and type-1 vanilloid receptors.	aea	108-111	fatty acid amide hydrolase	Mus musculus	151-155
18329052-2	2008	N-arachidonoylethanolamine (anandamide, AEA), is a full agonist at both cannabinoid CB(1) receptors and "transient receptor potential vanilloid" type 1 (TRPV1) channels, and N-palmitoylethanolamine (PEA) potentiates these effects.	aea	0-26	transient receptor potential cation channel subfamily V member 1	Homo sapiens	153-158
20525128-7	2008	Leukotriene C4 (LTC4) synthase is the enzyme responsible for the production of leukotriene C4, the chief cysteinyl leukotriene responsible for AEA.	aea	143-146	leukotriene C4 synthase	Homo sapiens	0-30
18571623-5	2008	Interestingly, the current studies also demonstrate that while the potency of 2-AG is comparable between human Jurkat T cells and murine splenocytes, anandamide (AEA) is markedly more potent in suppressing IL-2 production in Jurkat T cells compared to murine splenocytes.	aea	162-165	interleukin 2	Mus musculus	206-210
18571623-8	2008	These studies suggest that the potency of AEA in the suppression of IL-2 secretion may correlate with COX-2 protein levels in different T cell models.	aea	42-45	interleukin 2	Homo sapiens	68-72
18571623-8	2008	These studies suggest that the potency of AEA in the suppression of IL-2 secretion may correlate with COX-2 protein levels in different T cell models.	aea	42-45	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	102-107
20525128-9	2008	An allele of the LTC4 synthase gene in AEA is known as allele C. Allele C has a higher frequency in AEA.	aea	39-42	leukotriene C4 synthase	Homo sapiens	17-30
20525128-9	2008	An allele of the LTC4 synthase gene in AEA is known as allele C. Allele C has a higher frequency in AEA.	aea	100-103	leukotriene C4 synthase	Homo sapiens	17-30
17921459-4	2008	When AEA contents in the PFC were increased by microinjecting the selective inhibitor of fatty acid amide hydrolase (FAAH), URB597, we observed an anxiolytic response only at low doses of the compound and no effect or even an anxiogenic profile at higher doses.	aea	5-8	fatty-acid amide hydrolase-like	Rattus norvegicus	117-121
17921459-5	2008	In line with this, a marked decrease of AEA levels in the PFC, achieved by lentivirus-mediated local overexpression of FAAH, produced an anxiogenic response.	aea	40-43	fatty-acid amide hydrolase-like	Rattus norvegicus	119-123
17921459-3	2008	Pretreatment with the selective antagonist of CB1 or TRPV1 receptors (AM251 and capsazepine, respectively) suggested that the anxiolytic effect evoked by AEA might be due to the interaction with the CB1 cannabinoid receptor, whereas vanilloid receptors seem to be involved in AEA anxiogenic action.	aea	154-157	cannabinoid receptor 1	Rattus norvegicus	46-49
18376419-10	2008	Preincubating DRG neurons with the fatty acid amide hydrolase (FAAH) inhibitor phenylmethylsulphonyl fluoride (PMSF) attenuated the inhibitory actions of AEA on K(+) currents and Ca(2+) influx.	aea	154-157	fatty-acid amide hydrolase-like	Rattus norvegicus	35-61
17921459-3	2008	Pretreatment with the selective antagonist of CB1 or TRPV1 receptors (AM251 and capsazepine, respectively) suggested that the anxiolytic effect evoked by AEA might be due to the interaction with the CB1 cannabinoid receptor, whereas vanilloid receptors seem to be involved in AEA anxiogenic action.	aea	154-157	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	53-58
17921459-3	2008	Pretreatment with the selective antagonist of CB1 or TRPV1 receptors (AM251 and capsazepine, respectively) suggested that the anxiolytic effect evoked by AEA might be due to the interaction with the CB1 cannabinoid receptor, whereas vanilloid receptors seem to be involved in AEA anxiogenic action.	aea	154-157	cannabinoid receptor 1	Rattus norvegicus	199-202
17921459-3	2008	Pretreatment with the selective antagonist of CB1 or TRPV1 receptors (AM251 and capsazepine, respectively) suggested that the anxiolytic effect evoked by AEA might be due to the interaction with the CB1 cannabinoid receptor, whereas vanilloid receptors seem to be involved in AEA anxiogenic action.	aea	276-279	cannabinoid receptor 1	Rattus norvegicus	46-49
17921459-3	2008	Pretreatment with the selective antagonist of CB1 or TRPV1 receptors (AM251 and capsazepine, respectively) suggested that the anxiolytic effect evoked by AEA might be due to the interaction with the CB1 cannabinoid receptor, whereas vanilloid receptors seem to be involved in AEA anxiogenic action.	aea	276-279	cannabinoid receptor 1	Rattus norvegicus	199-202
18376419-10	2008	Preincubating DRG neurons with the fatty acid amide hydrolase (FAAH) inhibitor phenylmethylsulphonyl fluoride (PMSF) attenuated the inhibitory actions of AEA on K(+) currents and Ca(2+) influx.	aea	154-157	fatty-acid amide hydrolase-like	Rattus norvegicus	63-67
17965731-1	2008	BACKGROUND AND PURPOSE: N-arachidonoyl ethanolamine (AEA) and 2-arachidonoyl glycerol (2-AG) are endogenous cannabinoids binding to the cannabinoid receptors CB1 and CB2 to modulate neuronal excitability and synaptic transmission in primary afferent neurons.	aea	24-51	cannabinoid receptor 1	Homo sapiens	158-161
17965731-10	2008	The observed co-localization of AEA, 2-AG, and their synthetic enzymes with the reported localization of CB1 raises the possibility of intrinsic-autocrine signalling within lipid raft domains and/or retrograde-paracrine signalling.	aea	32-35	cannabinoid receptor 1	Homo sapiens	105-108
17965731-1	2008	BACKGROUND AND PURPOSE: N-arachidonoyl ethanolamine (AEA) and 2-arachidonoyl glycerol (2-AG) are endogenous cannabinoids binding to the cannabinoid receptors CB1 and CB2 to modulate neuronal excitability and synaptic transmission in primary afferent neurons.	aea	24-51	cannabinoid receptor 2	Homo sapiens	166-169
17965731-1	2008	BACKGROUND AND PURPOSE: N-arachidonoyl ethanolamine (AEA) and 2-arachidonoyl glycerol (2-AG) are endogenous cannabinoids binding to the cannabinoid receptors CB1 and CB2 to modulate neuronal excitability and synaptic transmission in primary afferent neurons.	aea	53-56	cannabinoid receptor 1	Homo sapiens	158-161
17965731-1	2008	BACKGROUND AND PURPOSE: N-arachidonoyl ethanolamine (AEA) and 2-arachidonoyl glycerol (2-AG) are endogenous cannabinoids binding to the cannabinoid receptors CB1 and CB2 to modulate neuronal excitability and synaptic transmission in primary afferent neurons.	aea	53-56	cannabinoid receptor 2	Homo sapiens	166-169
17965731-6	2008	KEY RESULTS: Under basal conditions, the endogenous cannabinoid AEA was present in both lipid raft and specific non-lipid raft fractions as was one of its biosynthetic enzymes, NAPE-PLD.	aea	64-67	N-acyl phosphatidylethanolamine phospholipase D	Homo sapiens	177-185
17553686-3	2007	We assayed peripheral lymphocytes from HD patients and healthy controls, and found that the activity of the fatty acid amide hydrolase (FAAH), the enzyme that degrades the endocannabinoid anandamide (AEA), was dramatically decreased (down to less than 10%) in HD compared to healthy subjects.	aea	200-203	fatty acid amide hydrolase	Homo sapiens	108-134
17675189-2	2008	On the other hand, genetic deletion of fatty acid amide hydrolase (FAAH), the enzyme responsible for degradation of fatty acid amides, including endogenous cannabinoid N-arachidonoyl ethanolamine (anandamide; AEA), N-palmitoyl ethanolamine (PEA), N-oleoyl ethanolamine (OEA), and oleamide, also elicits anti-edema, but does not produce any apparent cannabinoid effects.	aea	168-195	fatty acid amide hydrolase	Mus musculus	50-65
17675189-2	2008	On the other hand, genetic deletion of fatty acid amide hydrolase (FAAH), the enzyme responsible for degradation of fatty acid amides, including endogenous cannabinoid N-arachidonoyl ethanolamine (anandamide; AEA), N-palmitoyl ethanolamine (PEA), N-oleoyl ethanolamine (OEA), and oleamide, also elicits anti-edema, but does not produce any apparent cannabinoid effects.	aea	168-195	fatty acid amide hydrolase	Mus musculus	67-71
17901541-10	2007	These studies support the hypothesis that the cellular AEA accumulation beyond simple equilibrium between intracellular and extracellular concentrations occurs because AEA binds to an intracellular protein that is not FAAH but that also recognizes the AEA uptake inhibitors.	aea	55-58	fatty acid amide hydrolase	Homo sapiens	218-222
17901541-10	2007	These studies support the hypothesis that the cellular AEA accumulation beyond simple equilibrium between intracellular and extracellular concentrations occurs because AEA binds to an intracellular protein that is not FAAH but that also recognizes the AEA uptake inhibitors.	aea	168-171	fatty acid amide hydrolase	Homo sapiens	218-222
17901541-10	2007	These studies support the hypothesis that the cellular AEA accumulation beyond simple equilibrium between intracellular and extracellular concentrations occurs because AEA binds to an intracellular protein that is not FAAH but that also recognizes the AEA uptake inhibitors.	aea	168-171	fatty acid amide hydrolase	Homo sapiens	218-222
17553686-3	2007	We assayed peripheral lymphocytes from HD patients and healthy controls, and found that the activity of the fatty acid amide hydrolase (FAAH), the enzyme that degrades the endocannabinoid anandamide (AEA), was dramatically decreased (down to less than 10%) in HD compared to healthy subjects.	aea	200-203	fatty acid amide hydrolase	Homo sapiens	136-140
17259073-3	2007	Anandamide (N-arachidonoylethanolamine) and 2-AG (2-arachidonoylglycerol) are two major endocannabinoids that bind to and activate G-protein coupled cannabinoid receptors CB1 and CB2.	aea	12-38	cannabinoid receptor 1 (brain)	Mus musculus	171-174
17110429-8	2007	Finally, we demonstrate that FSH protects Sertoli cells against the pro-apoptotic activity of AEA, through PKA and aromatase-dependent activation of FAAH.	aea	94-97	fatty acid amide hydrolase	Mus musculus	149-153
17259073-3	2007	Anandamide (N-arachidonoylethanolamine) and 2-AG (2-arachidonoylglycerol) are two major endocannabinoids that bind to and activate G-protein coupled cannabinoid receptors CB1 and CB2.	aea	12-38	cannabinoid receptor 2 (macrophage)	Mus musculus	179-182
16375688-2	2005	The discovery of N-arachidonoylethanolamine (anandamide, AEA) and of the enzyme that terminates its signaling, i. e. fatty acid amide hydrolase (FAAH), has inspired pharmacological strategies to augment endocannabinoid tone and biological activity through inhibition of FAAH.	aea	17-43	fatty acid amide hydrolase	Homo sapiens	145-149
16448676-2	2006	Mice lacking the enzyme fatty acid amidohydrolase (FAAH) are severely impaired in their ability to degrade anandamide (AEA) and therefore represent a unique animal model in which to examine the function of AEA in vivo on ethanol-drinking behavior.	aea	119-122	fatty acid amide hydrolase	Mus musculus	51-55
16448676-2	2006	Mice lacking the enzyme fatty acid amidohydrolase (FAAH) are severely impaired in their ability to degrade anandamide (AEA) and therefore represent a unique animal model in which to examine the function of AEA in vivo on ethanol-drinking behavior.	aea	206-209	fatty acid amide hydrolase	Mus musculus	51-55
16448676-8	2006	Supersensitivity to exogenous AEA was noted in both male and female FAAH(-/-) mice.	aea	30-33	fatty acid amide hydrolase	Mus musculus	68-72
16548785-8	2006	The targets include the anandamide-hydrolysing enzyme fatty acid amide hydrolase, the carrier-mediated anandamide transport system and 2-arachidonoyl glycerol-deactivating enzyme monoacylglycerol lipase.	aea	24-34	monoglyceride lipase	Homo sapiens	179-202
17118807-4	2006	Cannabinoid type-1 (CB1) and CB2 receptors belong to the family of G protein-coupled receptors and are the primary targets of the endogenous cannabinoids N-arachidonoyl ethanolamine and 2-arachidonoyl glyerol.	aea	154-181	cannabinoid receptor 1	Homo sapiens	20-23
17118807-4	2006	Cannabinoid type-1 (CB1) and CB2 receptors belong to the family of G protein-coupled receptors and are the primary targets of the endogenous cannabinoids N-arachidonoyl ethanolamine and 2-arachidonoyl glyerol.	aea	154-181	cannabinoid receptor 2	Homo sapiens	29-32
16387640-4	2006	In this study, we show that the endocannabinoid system is highly activated during CNS inflammation and that the endocannabinoid anandamide (AEA) protects neurons from inflammatory damage by CB(1/2) receptor-mediated rapid induction of mitogen-activated protein kinase phosphatase-1 (MKP-1) in microglial cells associated with histone H3 phoshorylation of the mkp-1 gene sequence.	aea	140-143	dual specificity phosphatase 1	Homo sapiens	235-281
16387640-4	2006	In this study, we show that the endocannabinoid system is highly activated during CNS inflammation and that the endocannabinoid anandamide (AEA) protects neurons from inflammatory damage by CB(1/2) receptor-mediated rapid induction of mitogen-activated protein kinase phosphatase-1 (MKP-1) in microglial cells associated with histone H3 phoshorylation of the mkp-1 gene sequence.	aea	140-143	dual specificity phosphatase 1	Homo sapiens	283-288
16387640-4	2006	In this study, we show that the endocannabinoid system is highly activated during CNS inflammation and that the endocannabinoid anandamide (AEA) protects neurons from inflammatory damage by CB(1/2) receptor-mediated rapid induction of mitogen-activated protein kinase phosphatase-1 (MKP-1) in microglial cells associated with histone H3 phoshorylation of the mkp-1 gene sequence.	aea	140-143	dual specificity phosphatase 1	Homo sapiens	359-364
16387640-5	2006	As a result, AEA-induced rapid MKP-1 expression switches off MAPK signal transduction in microglial cells activated by stimulation of pattern recognition receptors.	aea	13-16	dual specificity phosphatase 1	Homo sapiens	31-36
16375688-2	2005	The discovery of N-arachidonoylethanolamine (anandamide, AEA) and of the enzyme that terminates its signaling, i. e. fatty acid amide hydrolase (FAAH), has inspired pharmacological strategies to augment endocannabinoid tone and biological activity through inhibition of FAAH.	aea	17-43	fatty acid amide hydrolase	Homo sapiens	270-274
15961786-4	2005	The present work studies the effect of AEA-induced structural modifications of the dipalmitoylphosphatidylcholine (DPPC) bilayer on phospholipase A2 (PLA2) activity, which is strictly dependent on lipid bilayer features.	aea	39-42	phospholipase A2 group IB	Homo sapiens	132-148
15961786-4	2005	The present work studies the effect of AEA-induced structural modifications of the dipalmitoylphosphatidylcholine (DPPC) bilayer on phospholipase A2 (PLA2) activity, which is strictly dependent on lipid bilayer features.	aea	39-42	phospholipase A2 group IB	Homo sapiens	150-154
15961786-5	2005	This study, performed by 2-dimethylamino-(6-lauroyl)-naphthalene fluorescence, demonstrates that the effect of AEA on PLA2 activity is concentration-dependent.	aea	111-114	phospholipase A2 group IB	Homo sapiens	118-122
15961786-8	2005	Because the biphasic effect of increasing AEA concentrations on PLA2 activity is related to the induced modifications of membrane bilayer structural properties, we suggest that AEA-phospholipid interactions may be important to produce, at least in part, some of the similarly biphasic responses of some physiological activities to increasing concentrations of AEA.	aea	42-45	phospholipase A2 group IB	Homo sapiens	64-68
15961786-8	2005	Because the biphasic effect of increasing AEA concentrations on PLA2 activity is related to the induced modifications of membrane bilayer structural properties, we suggest that AEA-phospholipid interactions may be important to produce, at least in part, some of the similarly biphasic responses of some physiological activities to increasing concentrations of AEA.	aea	177-180	phospholipase A2 group IB	Homo sapiens	64-68
15961786-8	2005	Because the biphasic effect of increasing AEA concentrations on PLA2 activity is related to the induced modifications of membrane bilayer structural properties, we suggest that AEA-phospholipid interactions may be important to produce, at least in part, some of the similarly biphasic responses of some physiological activities to increasing concentrations of AEA.	aea	177-180	phospholipase A2 group IB	Homo sapiens	64-68
15760304-1	2005	In animal tissues, NAEs (N-acylethanolamines), including N-arachidonoylethanolamine (anandamide), are primarily formed from their corresponding NAPEs (N-acylphosphatidylethanolamines) by a phosphodiesterase of the PLD (phospholipase D) type (NAPE-PLD).	aea	57-83	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	214-217
15760304-1	2005	In animal tissues, NAEs (N-acylethanolamines), including N-arachidonoylethanolamine (anandamide), are primarily formed from their corresponding NAPEs (N-acylphosphatidylethanolamines) by a phosphodiesterase of the PLD (phospholipase D) type (NAPE-PLD).	aea	57-83	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	219-234
16099396-1	2005	The endocannabinoid anandamide (N-arachidonoylethanolamine) was proposed to be an extracellular retrograde messenger, which regulates excitability of neurons by cannabinoid CB1 receptor-dependent inhibition of neurotransmitter release.	aea	32-58	cannabinoid receptor 1	Homo sapiens	173-176
15992380-1	2005	The endocannabinoid anandamide (N-arachidonoylethanolamine) and other bioactive long-chain N-acylethanolamines are thought to be formed from their corresponding N-acylphosphatidylethanolamines by a specific phospholipase D (NAPE-PLD) in the brain as well as other tissues.	aea	32-58	N-acyl phosphatidylethanolamine phospholipase D	Rattus norvegicus	224-232
15576840-2	2005	Because fatty acid amide hydrolase (FAAH) regulates brain AEA content, the purpose of this study was to determine its role in the postmortal accumulation of AEA using FAAH null mice.	aea	58-61	fatty acid amide hydrolase	Mus musculus	8-34
16176062-1	2005	Anandamide (N-arachidonoylethanolamine, AEA) is the putative endogenous ligand for the CB1 receptor.	aea	12-38	cannabinoid receptor 1	Rattus norvegicus	87-90
15766717-2	2005	The anandamide (N-arachidonoylethanolamine, AEA), product released by NAPE-PLD from the N-arachidonoyl-phosphatidylethanolamine (NArPE) substrate, was separated using a C18 column eluted with methanol-water-acetic acid and was quantified with an external standard method.	aea	16-42	N-acyl phosphatidylethanolamine phospholipase D	Mus musculus	70-78
15667652-8	2005	Also, NGF and GDNF each augmented anandamide (AEA)- and arachidonyl-2-chloroethylamide (ACEA)-evoked CGRP release, while BDNF was without effect.	aea	46-49	nerve growth factor	Rattus norvegicus	6-9
15667652-8	2005	Also, NGF and GDNF each augmented anandamide (AEA)- and arachidonyl-2-chloroethylamide (ACEA)-evoked CGRP release, while BDNF was without effect.	aea	46-49	glial cell derived neurotrophic factor	Rattus norvegicus	14-18
15667652-10	2005	Furthermore, NGF and GDNF each altered the concentration-response function for CAP- and AEA-evoked CGRP release, increasing the Emax without altering the EC50 for either compound.	aea	88-91	nerve growth factor	Rattus norvegicus	13-16
15667652-10	2005	Furthermore, NGF and GDNF each altered the concentration-response function for CAP- and AEA-evoked CGRP release, increasing the Emax without altering the EC50 for either compound.	aea	88-91	glial cell derived neurotrophic factor	Rattus norvegicus	21-25
15667652-10	2005	Furthermore, NGF and GDNF each altered the concentration-response function for CAP- and AEA-evoked CGRP release, increasing the Emax without altering the EC50 for either compound.	aea	88-91	calcitonin-related polypeptide alpha	Rattus norvegicus	99-103
15760304-1	2005	In animal tissues, NAEs (N-acylethanolamines), including N-arachidonoylethanolamine (anandamide), are primarily formed from their corresponding NAPEs (N-acylphosphatidylethanolamines) by a phosphodiesterase of the PLD (phospholipase D) type (NAPE-PLD).	aea	57-83	N-acyl phosphatidylethanolamine phospholipase D	Homo sapiens	242-250
15576840-2	2005	Because fatty acid amide hydrolase (FAAH) regulates brain AEA content, the purpose of this study was to determine its role in the postmortal accumulation of AEA using FAAH null mice.	aea	58-61	fatty acid amide hydrolase	Mus musculus	36-40
15576840-2	2005	Because fatty acid amide hydrolase (FAAH) regulates brain AEA content, the purpose of this study was to determine its role in the postmortal accumulation of AEA using FAAH null mice.	aea	157-160	fatty acid amide hydrolase	Mus musculus	8-34
15576840-2	2005	Because fatty acid amide hydrolase (FAAH) regulates brain AEA content, the purpose of this study was to determine its role in the postmortal accumulation of AEA using FAAH null mice.	aea	157-160	fatty acid amide hydrolase	Mus musculus	36-40
15576840-3	2005	As expected, AEA content in immediately frozen brain tissue was significantly greater in FAAH-deficient (FAAH-/-) than in wild-type mice.	aea	13-16	fatty acid amide hydrolase	Mus musculus	89-93
15576840-4	2005	However, AEA content was significantly lower in brains from FAAH-/- mice at 5 and 24 h postmortem.	aea	9-12	fatty acid amide hydrolase	Mus musculus	60-64
15576840-5	2005	Similarly, wild-type mice treated in vivo with a FAAH inhibitor (URB532) had significantly lower brain AEA content 24 h postmortem compared with controls.	aea	103-106	fatty acid amide hydrolase	Mus musculus	49-53
15576840-6	2005	These data indicate that FAAH contributes significantly to the postmortal accumulation of AEA.	aea	90-93	fatty acid amide hydrolase	Mus musculus	25-29
15576840-9	2005	These data demonstrate that FAAH activity differentially affects AEA and OEA/PEA contents postmortem and suggest that AEA formation specifically occurs via an ethanolamine-dependent route postmortem.	aea	65-68	fatty acid amide hydrolase	Mus musculus	28-32
15576840-9	2005	These data demonstrate that FAAH activity differentially affects AEA and OEA/PEA contents postmortem and suggest that AEA formation specifically occurs via an ethanolamine-dependent route postmortem.	aea	118-121	fatty acid amide hydrolase	Mus musculus	28-32
15157693-1	2004	Although the N-arachidonoyl ethanolamine (anandamide) binds to cannabinoid receptors and has been implicated in the suppression of pain, its rapid catabolism in vivo by fatty acid amide hydrolase (FAAH) has presented a challenge in investigating the physiological functions of this endogenous cannabinoid.	aea	13-40	fatty acid amide hydrolase	Mus musculus	197-201
16596770-10	2005	As well as acting on CB1 and CB2 receptors, there is convincing evidence that anandamide can activate transient receptor potential vanilloid type 1 (TRPV1) receptors.	aea	78-88	cannabinoid receptor 1	Homo sapiens	21-24
16596770-10	2005	As well as acting on CB1 and CB2 receptors, there is convincing evidence that anandamide can activate transient receptor potential vanilloid type 1 (TRPV1) receptors.	aea	78-88	transient receptor potential cation channel subfamily V member 1	Homo sapiens	102-147
16596770-10	2005	As well as acting on CB1 and CB2 receptors, there is convincing evidence that anandamide can activate transient receptor potential vanilloid type 1 (TRPV1) receptors.	aea	78-88	transient receptor potential cation channel subfamily V member 1	Homo sapiens	149-154
15189359-2	2004	Here we show that the amount of anandamide (AEA) and 2-arachidonoylglycerol (2-AG), two endocannabinoids that have neuroprotective properties, increase in spinal cord of SOD1(G93A) transgenic mice.	aea	44-47	superoxide dismutase 1, soluble	Mus musculus	170-174
14645706-3	2003	One potentially important mechanism involves signaling between an evolutionarily conserved G protein-coupled protein cannabinoid receptor, CB1, that is expressed at high levels on the surface of the trophectoderm and anandamide (N-arachi-donoylethanolamine), an endocannabinoid ligand found to be produced at higher levels by the uterus before implantation and then down-regulated at the time of implantation.	aea	229-256	cannabinoid receptor 1	Homo sapiens	139-142
15129189-1	2004	Endocannabinoids, including 2-arachidonoylglycerol and anandamide (N-arachidonoylethanolamine; AEA), have neuroprotective effects in the brain through actions at CB1 receptors.	aea	67-93	cannabinoid receptor 1	Rattus norvegicus	162-165
14715265-2	2004	NAGly is a potent inhibitor of the fatty acid amide hydrolase (FAAH), the enzyme primarily responsible for the degradation of the endocannabinoid N-arachidonoyl-ethanolamine (anandamide), and was shown recently to elevate the blood levels of the this analgesic compound.	aea	146-173	fatty-acid amide hydrolase-like	Rattus norvegicus	63-67
11585048-1	2001	Fatty acid amide hydrolase (FAAH) is responsible for the hydrolysis of a number of important endogenous fatty acid amides, including the endogenous cannabimimetic agent anandamide (AEA), the sleep-inducing compound oleamide, and the putative anti-inflammatory agent palmitoylethanolamide (PEA).	aea	181-184	fatty acid amide hydrolase	Homo sapiens	28-32
12137909-1	2002	Anandamide (N-arachidonoylethanolamine), an arachidonic acid derivative, is an endogenous ligand for both the brain-type (CB1-R) and spleen-type (CB2-R) cannabinoid receptors.	aea	12-38	cannabinoid receptor 1 (brain)	Mus musculus	122-127
12137909-1	2002	Anandamide (N-arachidonoylethanolamine), an arachidonic acid derivative, is an endogenous ligand for both the brain-type (CB1-R) and spleen-type (CB2-R) cannabinoid receptors.	aea	12-38	cannabinoid receptor 2 (macrophage)	Mus musculus	146-151
11982628-1	2002	Anandamide (N-arachidonoylethanolamine, AEA) and 2-arachidonoylglycerol (2-AG) are the most active endocannabinoids at brain (CB1) cannabinoid receptors.	aea	12-38	cannabinoid receptor 1 (brain)	Mus musculus	126-129
12672243-2	2003	Inhibition of the metabolism of AEA, catalyzed by fatty acid amide hydrolase (FAAH), potentiates the actions of AEA in vivo and therefore may be a useful target for drug development.	aea	32-35	fatty-acid amide hydrolase 1	Cricetulus griseus	78-82
12672243-2	2003	Inhibition of the metabolism of AEA, catalyzed by fatty acid amide hydrolase (FAAH), potentiates the actions of AEA in vivo and therefore may be a useful target for drug development.	aea	112-115	fatty-acid amide hydrolase 1	Cricetulus griseus	78-82
12672243-3	2003	In the present study, we have investigated whether substitution of the headgroup of the endogenous alternative FAAH substrate palmitoylethanolamide (PEA) can result in the identification of novel compounds preventing AEA metabolism.	aea	217-220	fatty-acid amide hydrolase 1	Cricetulus griseus	111-115
12702205-8	2003	AEA revealed that many SNPs in TNF are poor markers of each other.	aea	0-3	tumor necrosis factor	Homo sapiens	31-34
10820223-7	2000	Similarly, replacement of the ethanolamine of AEA with 3-pyridinyl also results in a high-affinity inhibitor of both the transporter and FAAH.	aea	46-49	fatty acid amide hydrolase	Homo sapiens	137-141
10723075-8	2000	The competition studies with SR141716A, a CB1 receptor antagonist, and 2-arachidonylglycerol (2-AG) and anandamide (AnNH), known CB1 receptor agonists, all showed a substantial decrease in [(3)H]CP-55,940 binding in both strains of mice with a higher K(i) values in the DBA/2 mice.	aea	116-120	cannabinoid receptor 1 (brain)	Mus musculus	129-132
9703957-1	1998	Fatty acid amide hydrolase (FAAH) catalyzes the hydrolysis of bioactive fatty acid amides and esters such as the endogenous cannabinoid receptor ligands, anandamide (N-arachidonoyl-ethanolamine) and 2-arachidonoylglycerol, and the putative sleep inducing factor cis-9-octadecenoamide (oleamide).	aea	166-193	fatty-acid amide hydrolase-like	Rattus norvegicus	0-26
10428468-1	1999	The N-acylphosphatidylethanolamine-hydrolysing phospholipase D (NAPE-PLD) generates N-acylethanolamines, including N-arachidonoyl-ethanolamine (anandamide), that may be neuroprotective and analgesic.	aea	115-142	N-acyl phosphatidylethanolamine phospholipase D	Rattus norvegicus	4-62
10428468-1	1999	The N-acylphosphatidylethanolamine-hydrolysing phospholipase D (NAPE-PLD) generates N-acylethanolamines, including N-arachidonoyl-ethanolamine (anandamide), that may be neuroprotective and analgesic.	aea	115-142	N-acyl phosphatidylethanolamine phospholipase D	Rattus norvegicus	64-72
10336536-3	1999	We have synthesized two analogs of N-arachidonylethanolamine (AEA), arachidonylcyclopropylamide (ACPA) and arachidonyl-2-chloroethylamide (ACEA), that bind to the CB1 receptor with very high affinity (KI values of 2.2 +/- 0.4 nM and 1.4 +/- 0.3 nM, respectively) and to the CB2 receptor with low affinity (KI values of 0.7 +/- 0.01 microM and 3.1 +/- 1.0 microM, respectively).	aea	62-65	cannabinoid receptor 1	Homo sapiens	163-166
10336536-3	1999	We have synthesized two analogs of N-arachidonylethanolamine (AEA), arachidonylcyclopropylamide (ACPA) and arachidonyl-2-chloroethylamide (ACEA), that bind to the CB1 receptor with very high affinity (KI values of 2.2 +/- 0.4 nM and 1.4 +/- 0.3 nM, respectively) and to the CB2 receptor with low affinity (KI values of 0.7 +/- 0.01 microM and 3.1 +/- 1.0 microM, respectively).	aea	62-65	cannabinoid receptor 2	Homo sapiens	274-277
10336536-6	1999	Therefore, ACPA and ACEA are high-affinity agonists of the CB1 receptor but do not bind the CB2 receptor, suggesting that structural analogs of AEA can be designed with considerable selectivity for the CB1 receptor over the CB2 receptor.	aea	144-147	cannabinoid receptor 1	Homo sapiens	59-62
10336536-6	1999	Therefore, ACPA and ACEA are high-affinity agonists of the CB1 receptor but do not bind the CB2 receptor, suggesting that structural analogs of AEA can be designed with considerable selectivity for the CB1 receptor over the CB2 receptor.	aea	144-147	cannabinoid receptor 1	Homo sapiens	202-205
10336536-6	1999	Therefore, ACPA and ACEA are high-affinity agonists of the CB1 receptor but do not bind the CB2 receptor, suggesting that structural analogs of AEA can be designed with considerable selectivity for the CB1 receptor over the CB2 receptor.	aea	144-147	cannabinoid receptor 2	Homo sapiens	224-227
10084956-1	1999	Anandamide (N-arachidonoylethanolamine), an arachidonic acid derivative, is an endogenous ligand for both the brain-type (CB1-R) and spleen-type (CB2-R) cannabinoid receptors.	aea	12-38	cannabinoid receptor 1 (brain)	Mus musculus	122-127
10734181-1	2000	N-Arachidonoylethanolamine (AEA) is a proposed endogenous ligand of the central cannabinoid receptor (CB1).	aea	0-26	cannabinoid receptor 1	Homo sapiens	102-105
10734181-1	2000	N-Arachidonoylethanolamine (AEA) is a proposed endogenous ligand of the central cannabinoid receptor (CB1).	aea	28-31	cannabinoid receptor 1	Homo sapiens	102-105
10785538-4	2000	Both AEA and 2-AG bind to the neuronal form of the cannabinoid receptor (CB1).	aea	5-8	cannabinoid receptor 1	Homo sapiens	73-76
10469888-2	1999	N- Arachidonoylethanolamine (anandamide) and some of its polyunsaturated congeners have been found in mammalian brain and shown to activate the CB1 and, with a lower efficacy, CB2 cannabinoid receptor subtypes.	aea	0-27	cannabinoid receptor 1	Homo sapiens	144-147
10469888-2	1999	N- Arachidonoylethanolamine (anandamide) and some of its polyunsaturated congeners have been found in mammalian brain and shown to activate the CB1 and, with a lower efficacy, CB2 cannabinoid receptor subtypes.	aea	0-27	cannabinoid receptor 2	Homo sapiens	176-179
9703957-1	1998	Fatty acid amide hydrolase (FAAH) catalyzes the hydrolysis of bioactive fatty acid amides and esters such as the endogenous cannabinoid receptor ligands, anandamide (N-arachidonoyl-ethanolamine) and 2-arachidonoylglycerol, and the putative sleep inducing factor cis-9-octadecenoamide (oleamide).	aea	166-193	fatty-acid amide hydrolase-like	Rattus norvegicus	28-32
9108127-1	1997	Anandamide (N-arachidonoylethanolamine) is an endogenous ligand for both the brain-type (CB1-R) and spleen-type (CB2-R) cannabinoid receptors.	aea	12-38	cannabinoid receptor 1 (brain)	Mus musculus	89-94
9655859-1	1998	N-Arachidonylethanolamine (AEA), a putative endogenous agonist of neuronal (CB1) cannabinoid receptors, is a substrate for N-arachidonylethanolamine amidohydrolase (AEA amidohydrolase), a serine amidase present in cell membranes.	aea	27-30	cannabinoid receptor 1	Rattus norvegicus	76-79
9458889-6	1998	Because AEA is rapidly converted to arachidonic acid and ethanolamine in brain and liver by a fatty acid amide hydrolase (FAAH), we hypothesized that the vasodilatory effect of AEA results from its hydrolysis to arachidonic acid followed by enzymatic conversion to vasodilatory eicosanoids.	aea	8-11	fatty-acid amide hydrolase 1	Bos taurus	94-120
9458889-6	1998	Because AEA is rapidly converted to arachidonic acid and ethanolamine in brain and liver by a fatty acid amide hydrolase (FAAH), we hypothesized that the vasodilatory effect of AEA results from its hydrolysis to arachidonic acid followed by enzymatic conversion to vasodilatory eicosanoids.	aea	8-11	fatty-acid amide hydrolase 1	Bos taurus	122-126
9458889-6	1998	Because AEA is rapidly converted to arachidonic acid and ethanolamine in brain and liver by a fatty acid amide hydrolase (FAAH), we hypothesized that the vasodilatory effect of AEA results from its hydrolysis to arachidonic acid followed by enzymatic conversion to vasodilatory eicosanoids.	aea	177-180	fatty-acid amide hydrolase 1	Bos taurus	94-120
9458889-6	1998	Because AEA is rapidly converted to arachidonic acid and ethanolamine in brain and liver by a fatty acid amide hydrolase (FAAH), we hypothesized that the vasodilatory effect of AEA results from its hydrolysis to arachidonic acid followed by enzymatic conversion to vasodilatory eicosanoids.	aea	177-180	fatty-acid amide hydrolase 1	Bos taurus	122-126
9458889-9	1998	Inhibition of the FAAH with diazomethylarachidonyl ketone blocked both the metabolism of [3H]AEA and the relaxations to AEA.	aea	93-96	fatty-acid amide hydrolase 1	Bos taurus	18-22
9458889-9	1998	Inhibition of the FAAH with diazomethylarachidonyl ketone blocked both the metabolism of [3H]AEA and the relaxations to AEA.	aea	120-123	fatty-acid amide hydrolase 1	Bos taurus	18-22
8162452-1	1994	IgG from 18 patients with SLE, eight with the primary antiphospholipid syndrome and 19 controls was examined for its effect on thrombin-induced prostacyclin (PGI2) release from human umbilical vein endothelial cells in relation to both the titre of anticardiolipin (ACA) and antiendothelial activity (AEA) and clinical thrombotic events.	aea	301-304	coagulation factor II, thrombin	Homo sapiens	127-135
8670178-1	1996	Anandamide (arachidonoylethanolamide, AnNH) has been recently proposed as the endogenous ligand at the brain cannabinoid receptor CB1.	aea	38-42	cannabinoid receptor 1 (brain)	Mus musculus	130-133
8893848-4	1996	The thio analogs of both anandamide and (R)-methanandamide showed very weak affinity for CB1.	aea	25-35	cannabinoid receptor 1 (brain)	Mus musculus	89-92
8893848-8	1996	Notably, anandamide and (R)-methanandamide demonstrated high selectivity for the CB1 receptor.	aea	9-19	cannabinoid receptor 1 (brain)	Mus musculus	81-84
34916909-2	2021	One such endocannabinoid is N-arachidonoylethanolamine (anandamide, AEA), which is metabolized by fatty acid amide hydrolase (FAAH).	aea	28-54	fatty acid amide hydrolase	Mus musculus	109-124
34756920-3	2022	AChE is critical in regulating cholinergic signaling while FAAH catalyzes the inactivation of fatty acid signaling lipids including the endocannabinoid (eCB) N-arachidonylethanolamine (anandamide, AEA) and eCB-like metabolites (e.g., oleoylethanolamide, OEA).	aea	197-200	acetylcholinesterase (Cartwright blood group)	Homo sapiens	0-4
34756920-3	2022	AChE is critical in regulating cholinergic signaling while FAAH catalyzes the inactivation of fatty acid signaling lipids including the endocannabinoid (eCB) N-arachidonylethanolamine (anandamide, AEA) and eCB-like metabolites (e.g., oleoylethanolamide, OEA).	aea	197-200	fatty acid amide hydrolase	Homo sapiens	59-63
34282702-2	2021	N-Arachidonoylethanolamine (anandamide; AEA) and 2-arachidonoylglycerol (2-AG) represent two major endocannabinoids in the human body and they exert many of their cellular and organ system effects by activating the Gi/o protein-coupled, cannabinoid type 1 (CB1) and type 2 (CB2) receptors.	aea	0-26	cannabinoid receptor 1	Homo sapiens	257-260
34282702-2	2021	N-Arachidonoylethanolamine (anandamide; AEA) and 2-arachidonoylglycerol (2-AG) represent two major endocannabinoids in the human body and they exert many of their cellular and organ system effects by activating the Gi/o protein-coupled, cannabinoid type 1 (CB1) and type 2 (CB2) receptors.	aea	0-26	cannabinoid receptor 2	Homo sapiens	274-277
34282702-2	2021	N-Arachidonoylethanolamine (anandamide; AEA) and 2-arachidonoylglycerol (2-AG) represent two major endocannabinoids in the human body and they exert many of their cellular and organ system effects by activating the Gi/o protein-coupled, cannabinoid type 1 (CB1) and type 2 (CB2) receptors.	aea	40-43	cannabinoid receptor 1	Homo sapiens	257-260
34282702-2	2021	N-Arachidonoylethanolamine (anandamide; AEA) and 2-arachidonoylglycerol (2-AG) represent two major endocannabinoids in the human body and they exert many of their cellular and organ system effects by activating the Gi/o protein-coupled, cannabinoid type 1 (CB1) and type 2 (CB2) receptors.	aea	40-43	cannabinoid receptor 2	Homo sapiens	274-277
34780173-2	2021	Here we report TRPV1 channel activation by the endocannabinoid, anandamide (AEA), in a unique, peripheral binding site via extended MD simulations.	aea	76-79	transient receptor potential cation channel subfamily V member 1	Homo sapiens	15-20
34893921-3	2021	Preclinical and particularly animal research has been able to demonstrate that homozygosity for the fatty acid amide hydrolase (FAAH) C385A allele, similar to FAAH inhibition, is associated with elevated concentrations of anandamide (AEA) and facilitates extinction learning and extinction recall.	aea	234-237	fatty acid amide hydrolase	Homo sapiens	100-126
34893921-3	2021	Preclinical and particularly animal research has been able to demonstrate that homozygosity for the fatty acid amide hydrolase (FAAH) C385A allele, similar to FAAH inhibition, is associated with elevated concentrations of anandamide (AEA) and facilitates extinction learning and extinction recall.	aea	234-237	fatty acid amide hydrolase	Homo sapiens	128-132
34893921-3	2021	Preclinical and particularly animal research has been able to demonstrate that homozygosity for the fatty acid amide hydrolase (FAAH) C385A allele, similar to FAAH inhibition, is associated with elevated concentrations of anandamide (AEA) and facilitates extinction learning and extinction recall.	aea	234-237	fatty acid amide hydrolase	Homo sapiens	159-163
34916909-2	2021	One such endocannabinoid is N-arachidonoylethanolamine (anandamide, AEA), which is metabolized by fatty acid amide hydrolase (FAAH).	aea	28-54	fatty acid amide hydrolase	Mus musculus	126-130
34916909-2	2021	One such endocannabinoid is N-arachidonoylethanolamine (anandamide, AEA), which is metabolized by fatty acid amide hydrolase (FAAH).	aea	68-71	fatty acid amide hydrolase	Mus musculus	109-124
34916909-2	2021	One such endocannabinoid is N-arachidonoylethanolamine (anandamide, AEA), which is metabolized by fatty acid amide hydrolase (FAAH).	aea	68-71	fatty acid amide hydrolase	Mus musculus	126-130
34684588-8	2021	The hypothalamic immunoreactivity of cannabinoid receptor 1, agouti-related protein, and orexin-A was not affected by either treatment; however, neuropeptide Y and agouti-related protein mRNA abundances were downregulated in the arcuate nucleus of AEA-treated animals.	aea	248-251	cannabinoid receptor 1	Bos taurus	37-59
34684588-8	2021	The hypothalamic immunoreactivity of cannabinoid receptor 1, agouti-related protein, and orexin-A was not affected by either treatment; however, neuropeptide Y and agouti-related protein mRNA abundances were downregulated in the arcuate nucleus of AEA-treated animals.	aea	248-251	neuropeptide Y	Bos taurus	145-159
34684588-8	2021	The hypothalamic immunoreactivity of cannabinoid receptor 1, agouti-related protein, and orexin-A was not affected by either treatment; however, neuropeptide Y and agouti-related protein mRNA abundances were downregulated in the arcuate nucleus of AEA-treated animals.	aea	248-251	agouti related neuropeptide	Bos taurus	61-83
34684588-8	2021	The hypothalamic immunoreactivity of cannabinoid receptor 1, agouti-related protein, and orexin-A was not affected by either treatment; however, neuropeptide Y and agouti-related protein mRNA abundances were downregulated in the arcuate nucleus of AEA-treated animals.	aea	248-251	agouti related neuropeptide	Bos taurus	164-186
34684588-8	2021	The hypothalamic immunoreactivity of cannabinoid receptor 1, agouti-related protein, and orexin-A was not affected by either treatment; however, neuropeptide Y and agouti-related protein mRNA abundances were downregulated in the arcuate nucleus of AEA-treated animals.	aea	248-251	hypocretin neuropeptide precursor	Bos taurus	89-97
34280820-8	2021	RESULTS: Circulating concentrations of AEA and BDNF (but not 2-AG and HVA) were found to mediate the relationship between moderate-intensity aerobic exercise and reduced threat expectancy ratings following reinstatement (AEA 95% CI: -0.623 to -0.005; BDNF 95% CI: -0.941 to -0.005).	aea	39-42	brain derived neurotrophic factor	Homo sapiens	251-255
34293356-8	2021	Anandamide (AEA), 2AG, and AM404 reduced SCAP viability in all experimental periods at the highest concentration, compared with the group with no treatment.	aea	12-15	SREBF chaperone	Homo sapiens	41-45
34280820-8	2021	RESULTS: Circulating concentrations of AEA and BDNF (but not 2-AG and HVA) were found to mediate the relationship between moderate-intensity aerobic exercise and reduced threat expectancy ratings following reinstatement (AEA 95% CI: -0.623 to -0.005; BDNF 95% CI: -0.941 to -0.005).	aea	221-224	brain derived neurotrophic factor	Homo sapiens	47-51
34587978-5	2021	In the 5xFAD model, the genetic inactivation of the enzyme that degrades anandamide (AEA), the fatty acid amide hydrolase (FAAH), was associated with a significant amelioration of the memory deficit.	aea	85-88	fatty acid amide hydrolase	Mus musculus	95-121
34587978-5	2021	In the 5xFAD model, the genetic inactivation of the enzyme that degrades anandamide (AEA), the fatty acid amide hydrolase (FAAH), was associated with a significant amelioration of the memory deficit.	aea	85-88	fatty acid amide hydrolase	Mus musculus	123-127
34217798-6	2021	In order to modulate endocannabinoid system, number of agents have been reported amongst which are inhibitors of the monoacylglycerol (MAGL) and fatty acid amide hydrolase (FAAH), the enzymes that hydrolyses 2-AG and AEA respectively.	aea	217-220	monoglyceride lipase	Homo sapiens	135-139
34522703-6	2021	Therefore, we tested the hypothesis that intra-BLA injection of a diacylglycerol lipase (DAGL) inhibitor (which would be expected to reduce 2-AG levels in BLA) and intra-CeA injection of a fatty acid amide hydrolase (FAAH) inhibitor (which would be expected to increase AEA levels in CeA) would mimic previously observed predator odor stress-induced reductions in ASR.	aea	270-273	fatty-acid amide hydrolase-like	Rattus norvegicus	217-221
34217798-6	2021	In order to modulate endocannabinoid system, number of agents have been reported amongst which are inhibitors of the monoacylglycerol (MAGL) and fatty acid amide hydrolase (FAAH), the enzymes that hydrolyses 2-AG and AEA respectively.	aea	217-220	fatty acid amide hydrolase	Homo sapiens	145-171
34217798-6	2021	In order to modulate endocannabinoid system, number of agents have been reported amongst which are inhibitors of the monoacylglycerol (MAGL) and fatty acid amide hydrolase (FAAH), the enzymes that hydrolyses 2-AG and AEA respectively.	aea	217-220	fatty acid amide hydrolase	Homo sapiens	173-177
34435626-1	2021	The fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) enzymes are the predominant catabolic regulators of the major endocannabinoids (eCBs) anadamide (AEA) and 2-arachidonoylglycerol (2-AG), respectively.	aea	170-173	fatty-acid amide hydrolase 1	Danio rerio	32-36
34299330-2	2021	Since the inhibition of fatty acid amide hydrolase (FAAH), the main catabolic enzyme of anandamide (AEA), may provide beneficial effects in mice model of Alzheimer"s disease (AD)-like pathology, we aimed at determining whether the FAAH inhibitor URB597 might target microglia polarization and alter the cytoskeleton reorganization induced by the amyloid-beta peptide (Abeta).	aea	100-103	fatty acid amide hydrolase	Mus musculus	24-50
34435626-1	2021	The fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) enzymes are the predominant catabolic regulators of the major endocannabinoids (eCBs) anadamide (AEA) and 2-arachidonoylglycerol (2-AG), respectively.	aea	170-173	fatty-acid amide hydrolase 1	Danio rerio	4-30
34360541-2	2021	Therefore, we determined whether human corneal epithelial cells (HCECs) express members of the endocannabinoid system (ECS), and examined how the endocannabinoid anandamide (AEA, N-arachidonoyl ethanolamine) influences the Toll-like receptor 3 (TLR3) agonism- or UVB irradiation-induced inflammatory response of these cells.	aea	174-177	toll like receptor 3	Homo sapiens	223-243
34360541-2	2021	Therefore, we determined whether human corneal epithelial cells (HCECs) express members of the endocannabinoid system (ECS), and examined how the endocannabinoid anandamide (AEA, N-arachidonoyl ethanolamine) influences the Toll-like receptor 3 (TLR3) agonism- or UVB irradiation-induced inflammatory response of these cells.	aea	174-177	toll like receptor 3	Homo sapiens	245-249
34360541-2	2021	Therefore, we determined whether human corneal epithelial cells (HCECs) express members of the endocannabinoid system (ECS), and examined how the endocannabinoid anandamide (AEA, N-arachidonoyl ethanolamine) influences the Toll-like receptor 3 (TLR3) agonism- or UVB irradiation-induced inflammatory response of these cells.	aea	179-206	toll like receptor 3	Homo sapiens	223-243
34360541-2	2021	Therefore, we determined whether human corneal epithelial cells (HCECs) express members of the endocannabinoid system (ECS), and examined how the endocannabinoid anandamide (AEA, N-arachidonoyl ethanolamine) influences the Toll-like receptor 3 (TLR3) agonism- or UVB irradiation-induced inflammatory response of these cells.	aea	179-206	toll like receptor 3	Homo sapiens	245-249
34126378-9	2021	Moreover, AEA induced an increase in caspase -3/-7 activities in both cell models, but in hGCs there was also an increase in caspase 8 activity.	aea	10-13	caspase 3	Homo sapiens	37-50
34126378-9	2021	Moreover, AEA induced an increase in caspase -3/-7 activities in both cell models, but in hGCs there was also an increase in caspase 8 activity.	aea	10-13	caspase 8	Homo sapiens	125-134
34299330-2	2021	Since the inhibition of fatty acid amide hydrolase (FAAH), the main catabolic enzyme of anandamide (AEA), may provide beneficial effects in mice model of Alzheimer"s disease (AD)-like pathology, we aimed at determining whether the FAAH inhibitor URB597 might target microglia polarization and alter the cytoskeleton reorganization induced by the amyloid-beta peptide (Abeta).	aea	100-103	fatty acid amide hydrolase	Mus musculus	52-56
35532037-6	2022	CRP correlated positively with AEA, and AEA showed positive associations with 2-AG and NAE levels.	aea	31-34	C-reactive protein	Homo sapiens	0-3
35482948-1	2022	Anandamide or N-arachidonoylethanolamine (AEA) is a signaling lipid that modulates neurotransmitter release via activation of the type 1 cannabinoid receptor (CB1R) in the brain.	aea	14-40	cannabinoid receptor 1 (brain)	Mus musculus	159-163
35482948-1	2022	Anandamide or N-arachidonoylethanolamine (AEA) is a signaling lipid that modulates neurotransmitter release via activation of the type 1 cannabinoid receptor (CB1R) in the brain.	aea	42-45	cannabinoid receptor 1 (brain)	Mus musculus	159-163
34061772-11	2021	However, AEA levels were negatively influenced by ACTH and copeptin levels, while OEA levels were negatively predicted by copeptin levels only.	aea	9-12	proopiomelanocortin	Homo sapiens	50-54
34061772-11	2021	However, AEA levels were negatively influenced by ACTH and copeptin levels, while OEA levels were negatively predicted by copeptin levels only.	aea	9-12	arginine vasopressin	Homo sapiens	59-67
35112235-11	2022	Furthermore, the group received AEA showed a decrease in the expressions of CREB and p-CREB possibly through the activation of the CB1 and TRPV1 receptors.	aea	32-35	cAMP responsive element binding protein 1	Rattus norvegicus	76-80
35112235-11	2022	Furthermore, the group received AEA showed a decrease in the expressions of CREB and p-CREB possibly through the activation of the CB1 and TRPV1 receptors.	aea	32-35	cAMP responsive element binding protein 1	Rattus norvegicus	87-91
35112235-11	2022	Furthermore, the group received AEA showed a decrease in the expressions of CREB and p-CREB possibly through the activation of the CB1 and TRPV1 receptors.	aea	32-35	cannabinoid receptor 1	Rattus norvegicus	131-134
35112235-11	2022	Furthermore, the group received AEA showed a decrease in the expressions of CREB and p-CREB possibly through the activation of the CB1 and TRPV1 receptors.	aea	32-35	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	139-144
35112235-12	2022	Activation of CB1 and TRPV1 receptors might be involved in AEA anticonvulsant effect in kindling model of epilepsy.	aea	59-62	cannabinoid receptor 1	Rattus norvegicus	14-17
35112235-12	2022	Activation of CB1 and TRPV1 receptors might be involved in AEA anticonvulsant effect in kindling model of epilepsy.	aea	59-62	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	22-27
35413977-8	2022	Western blot analyses revealed increased expression of Smad3 protein levels in the kidney cortex in response to chronic treatment with a high AEA dose.	aea	142-145	SMAD family member 3	Rattus norvegicus	55-60
35490598-5	2022	Transcript analysis of angiogenic factors of the vascular endothelial growth factor (VEGF) and matrix metalloproteinase (MMP) protein family demonstrated the ability of AEA to increase VEGF-C and VEGFR3 expression via cannabinoid receptors CB1 and CB2 while the placental growth factor (PlGF) was increased through CB1.	aea	169-172	vascular endothelial growth factor A	Homo sapiens	49-83
35490598-5	2022	Transcript analysis of angiogenic factors of the vascular endothelial growth factor (VEGF) and matrix metalloproteinase (MMP) protein family demonstrated the ability of AEA to increase VEGF-C and VEGFR3 expression via cannabinoid receptors CB1 and CB2 while the placental growth factor (PlGF) was increased through CB1.	aea	169-172	vascular endothelial growth factor A	Homo sapiens	85-89
35490598-5	2022	Transcript analysis of angiogenic factors of the vascular endothelial growth factor (VEGF) and matrix metalloproteinase (MMP) protein family demonstrated the ability of AEA to increase VEGF-C and VEGFR3 expression via cannabinoid receptors CB1 and CB2 while the placental growth factor (PlGF) was increased through CB1.	aea	169-172	matrix metallopeptidase 2	Homo sapiens	121-124
35490598-5	2022	Transcript analysis of angiogenic factors of the vascular endothelial growth factor (VEGF) and matrix metalloproteinase (MMP) protein family demonstrated the ability of AEA to increase VEGF-C and VEGFR3 expression via cannabinoid receptors CB1 and CB2 while the placental growth factor (PlGF) was increased through CB1.	aea	169-172	vascular endothelial growth factor C	Homo sapiens	185-191
35490598-5	2022	Transcript analysis of angiogenic factors of the vascular endothelial growth factor (VEGF) and matrix metalloproteinase (MMP) protein family demonstrated the ability of AEA to increase VEGF-C and VEGFR3 expression via cannabinoid receptors CB1 and CB2 while the placental growth factor (PlGF) was increased through CB1.	aea	169-172	fms related receptor tyrosine kinase 4	Homo sapiens	196-202
35490598-5	2022	Transcript analysis of angiogenic factors of the vascular endothelial growth factor (VEGF) and matrix metalloproteinase (MMP) protein family demonstrated the ability of AEA to increase VEGF-C and VEGFR3 expression via cannabinoid receptors CB1 and CB2 while the placental growth factor (PlGF) was increased through CB1.	aea	169-172	cannabinoid receptor 1	Homo sapiens	240-243
35490598-5	2022	Transcript analysis of angiogenic factors of the vascular endothelial growth factor (VEGF) and matrix metalloproteinase (MMP) protein family demonstrated the ability of AEA to increase VEGF-C and VEGFR3 expression via cannabinoid receptors CB1 and CB2 while the placental growth factor (PlGF) was increased through CB1.	aea	169-172	cannabinoid receptor 2	Homo sapiens	248-251
35490598-5	2022	Transcript analysis of angiogenic factors of the vascular endothelial growth factor (VEGF) and matrix metalloproteinase (MMP) protein family demonstrated the ability of AEA to increase VEGF-C and VEGFR3 expression via cannabinoid receptors CB1 and CB2 while the placental growth factor (PlGF) was increased through CB1.	aea	169-172	placental growth factor	Homo sapiens	262-285
35490598-5	2022	Transcript analysis of angiogenic factors of the vascular endothelial growth factor (VEGF) and matrix metalloproteinase (MMP) protein family demonstrated the ability of AEA to increase VEGF-C and VEGFR3 expression via cannabinoid receptors CB1 and CB2 while the placental growth factor (PlGF) was increased through CB1.	aea	169-172	placental growth factor	Homo sapiens	287-291
35490598-5	2022	Transcript analysis of angiogenic factors of the vascular endothelial growth factor (VEGF) and matrix metalloproteinase (MMP) protein family demonstrated the ability of AEA to increase VEGF-C and VEGFR3 expression via cannabinoid receptors CB1 and CB2 while the placental growth factor (PlGF) was increased through CB1.	aea	169-172	cannabinoid receptor 1	Homo sapiens	315-318
35490598-10	2022	Moreover, the data demonstrated that both AEA and 2-AG, via cannabinoid receptors, activated the STAT3 signaling pathway.	aea	42-45	signal transducer and activator of transcription 3	Homo sapiens	97-102
35436517-9	2022	This confirms that CB1 actually mediate the amnestic effect caused by the augmented AEA pool, but TRPV1 does not.	aea	84-87	cannabinoid receptor 1	Rattus norvegicus	19-22
35413977-9	2022	Therefore, TGF-beta1/Smad3 signaling pathway may play a crucial role in kidney injury in SS hypertension during chronic treatment with AEA.	aea	135-138	transforming growth factor, beta 1	Rattus norvegicus	11-20
35413977-9	2022	Therefore, TGF-beta1/Smad3 signaling pathway may play a crucial role in kidney injury in SS hypertension during chronic treatment with AEA.	aea	135-138	SMAD family member 3	Rattus norvegicus	21-26
35316021-4	2022	While MAGL inhibitors upregulate 2-acyl glycerol (2-AG) levels and reduce neuroinflammation, FAAH inhibitors elevate anandamide (AEA) levels and prevent the degradation of HSP-70, thereby preventing the phosphorylation of tau protein and formation of NFTs in neural cells.	aea	129-132	fatty acid amide hydrolase	Mus musculus	93-97
35395682-3	2022	Endocannabinoids (eCBs) including 2-arachidonyl glycerol (2-AG) and anandamide (AEA), are bioactive lipids that activate cannabinoid receptor, CB1, to regulate synaptic transmission and mediate cognitive functions and many behaviors, including sleep.	aea	80-83	cannabinoid receptor 1 (brain)	Mus musculus	143-146
35263737-7	2022	AEA analog palmitoylethanolamide (PEA) is also associated positively with the yearly change in eGFR.	aea	0-3	epidermal growth factor receptor	Homo sapiens	95-99
35190698-5	2022	In neonatal rat cardiomyocytes, RSG increased the level of anandamide (AEA); upregulated the expression of N-acyl phosphatidylethanolamine phospholipase D (NapePLD), a key enzyme for AEA synthesis; and downregulated the expression of fatty acid amide hydrolase (FAAH), the enzyme responsible for the degradation of AEA.	aea	183-186	N-acyl phosphatidylethanolamine phospholipase D	Rattus norvegicus	107-154
34995983-9	2022	FAAH, the principal hydrolytic enzyme for arachidonoylethanolamide (anandamide, AEA), catalyzes the hydrolysis of all three isomers with similar efficiencies.	aea	80-83	fatty acid amide hydrolase	Homo sapiens	0-4
34983657-4	2022	FAAH-1 is the primary enzyme accountable for the degradation of AEA and related fatty acid amides.	aea	64-67	fatty acid amide hydrolase	Homo sapiens	0-6
33722705-5	2021	Considering this, our work aims to clarify the molecular mechanisms underlying the anti-cancer properties of the endocannabinoid anandamide (AEA) and of the phytocannabinoids, cannabidiol (CBD) and Delta9-tetrahydrocannabinol (THC), in estrogen receptor-positive (ER+) breast cancer cells that overexpress aromatase (MCF-7aro).	aea	141-144	estrogen receptor 1	Homo sapiens	236-253
33915294-4	2021	Following their biosynthesis, AA and AEA can be further metabolized into additional eicosanoids, notably by the 15-lipoxygenase pathway.	aea	37-40	arachidonate 15-lipoxygenase	Homo sapiens	112-127
33722705-10	2021	On the other hand, AEA and CBD not only exhibited high anti-aromatase activity but also induced up-regulation of ERbeta.	aea	19-22	estrogen receptor 1	Homo sapiens	113-119
33722705-5	2021	Considering this, our work aims to clarify the molecular mechanisms underlying the anti-cancer properties of the endocannabinoid anandamide (AEA) and of the phytocannabinoids, cannabidiol (CBD) and Delta9-tetrahydrocannabinol (THC), in estrogen receptor-positive (ER+) breast cancer cells that overexpress aromatase (MCF-7aro).	aea	141-144	epiregulin	Homo sapiens	264-266
33886158-3	2021	The endocannabinoids (eCBs), 2-AG and AEA, which act at the primary cannabinoid receptor (CB1), mediate behaviors relevant to neurodevelopmental disorders.	aea	38-41	cannabinoid receptor 1 (brain)	Mus musculus	90-93
33995054-7	2021	Microarray data showed that AEA treatment in ARDS mice significantly altered numerous miRNA including downregulation of miRNA-23a-3p, which caused an upregulation of arginase (ARG1), which encodes for arginase, a marker for MDSCs, as well as TGF-beta2, which induces Tregs.	aea	28-31	arginase, liver	Mus musculus	176-180
33995054-7	2021	Microarray data showed that AEA treatment in ARDS mice significantly altered numerous miRNA including downregulation of miRNA-23a-3p, which caused an upregulation of arginase (ARG1), which encodes for arginase, a marker for MDSCs, as well as TGF-beta2, which induces Tregs.	aea	28-31	transforming growth factor, beta 2	Mus musculus	242-251
33995054-8	2021	AEA also caused down-regulation of miRNA-34a-5p which led to induction of FoxP3, a master regulator of Tregs.	aea	0-3	forkhead box P3	Mus musculus	74-79
33452437-8	2021	These alterations were accompanied by elevated hydrolytic activity of the enzyme fatty acid amide hydrolase (FAAH), which hydrolyzes the eCB anandamide (AEA), throughout multiple corticolimbic brain regions.	aea	153-156	fatty-acid amide hydrolase-like	Rattus norvegicus	81-107
33749884-3	2021	However, COX-2 is also able to metabolize other lipids, including the endocannabinoids 2-arachidonoylglycerol (2-AG) and anandamide (AEA), to give glycerol ester (PG-G) and ethanolamide (PG-EA) derivatives of the PGs.	aea	133-136	cytochrome c oxidase II, mitochondrial	Mus musculus	9-14
33070154-1	2021	JNJ-42165279 is a selective inhibitor of fatty acid amide hydrolase (FAAH), the enzyme responsible for the degradation of fatty acid amides (FAA) including anandamide (AEA), palmitoylethanolamide (PEA), and N-oleoylethanolamide (OEA).	aea	168-171	fatty acid amide hydrolase	Homo sapiens	41-67
33070154-1	2021	JNJ-42165279 is a selective inhibitor of fatty acid amide hydrolase (FAAH), the enzyme responsible for the degradation of fatty acid amides (FAA) including anandamide (AEA), palmitoylethanolamide (PEA), and N-oleoylethanolamide (OEA).	aea	168-171	fatty acid amide hydrolase	Homo sapiens	69-73
33834617-2	2021	Both FAAH and MAGL are the endocannabinoid degrading enzymes that hydrolyze several endogenous ligands, mainly anandamide (AEA) and 2-arachidonic glycerol (2-AG), which regulated the various pathophysiological condition of the body like emotion, cognition, energy balance, pain sensation, neuro-inflammation, and cancer cell proliferation.	aea	123-126	fatty acid amide hydrolase	Homo sapiens	5-9
33834617-2	2021	Both FAAH and MAGL are the endocannabinoid degrading enzymes that hydrolyze several endogenous ligands, mainly anandamide (AEA) and 2-arachidonic glycerol (2-AG), which regulated the various pathophysiological condition of the body like emotion, cognition, energy balance, pain sensation, neuro-inflammation, and cancer cell proliferation.	aea	123-126	monoglyceride lipase	Homo sapiens	14-18
33834617-3	2021	FAAH and MAGL inhibitors block the metabolism of AEA and 2-AG, and increases endogenous levels of fatty acid amides, and exert various therapeutic effects including chronic pain, metabolic disorders, psychoses, nausea and vomiting, depression, and anxiety disorders, etc.	aea	49-52	fatty acid amide hydrolase	Homo sapiens	0-4
33834617-3	2021	FAAH and MAGL inhibitors block the metabolism of AEA and 2-AG, and increases endogenous levels of fatty acid amides, and exert various therapeutic effects including chronic pain, metabolic disorders, psychoses, nausea and vomiting, depression, and anxiety disorders, etc.	aea	49-52	monoglyceride lipase	Homo sapiens	9-13
33797678-5	2022	It was observed that the HEp-2 LSCC cell line released AEA and 2-AG; the median quantity of AEA released was 15.69 ng mL-1 (range: 14.55-15.95 ng mL-1) and the median quantity of 2-AG released was 2.72 ng -1 (range: 2.67-2.74 ng mL-1).	aea	92-95	L1 cell adhesion molecule	Mus musculus	118-122
33607363-1	2021	As anandamide (N-arachidonoylethanolamine, AEA) shows neuroprotective effects, the inhibition of its degradative enzyme, fatty acid amide hydrolase (FAAH) has been considered as a hopeful avenue for the treatment of neurodegenerative diseases, like Alzheimer"s disease (AD).	aea	15-41	fatty acid amide hydrolase	Homo sapiens	121-147
33607363-1	2021	As anandamide (N-arachidonoylethanolamine, AEA) shows neuroprotective effects, the inhibition of its degradative enzyme, fatty acid amide hydrolase (FAAH) has been considered as a hopeful avenue for the treatment of neurodegenerative diseases, like Alzheimer"s disease (AD).	aea	15-41	fatty acid amide hydrolase	Homo sapiens	149-153
33607363-1	2021	As anandamide (N-arachidonoylethanolamine, AEA) shows neuroprotective effects, the inhibition of its degradative enzyme, fatty acid amide hydrolase (FAAH) has been considered as a hopeful avenue for the treatment of neurodegenerative diseases, like Alzheimer"s disease (AD).	aea	43-46	fatty acid amide hydrolase	Homo sapiens	121-147
33607363-1	2021	As anandamide (N-arachidonoylethanolamine, AEA) shows neuroprotective effects, the inhibition of its degradative enzyme, fatty acid amide hydrolase (FAAH) has been considered as a hopeful avenue for the treatment of neurodegenerative diseases, like Alzheimer"s disease (AD).	aea	43-46	fatty acid amide hydrolase	Homo sapiens	149-153
33514875-4	2021	We found that the endocannabinoid, anandamide (AEA), rather than 2-arachidonoylglycerol elicited glutamate release through presynaptic transient receptor potential vanilloid 1 (TRPV1) and astrocytic cannabinoid type-1 receptors (CB1Rs) in the NAcore of saline-yoked rats.	aea	47-50	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	135-175
33514875-4	2021	We found that the endocannabinoid, anandamide (AEA), rather than 2-arachidonoylglycerol elicited glutamate release through presynaptic transient receptor potential vanilloid 1 (TRPV1) and astrocytic cannabinoid type-1 receptors (CB1Rs) in the NAcore of saline-yoked rats.	aea	47-50	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	177-182
33452437-8	2021	These alterations were accompanied by elevated hydrolytic activity of the enzyme fatty acid amide hydrolase (FAAH), which hydrolyzes the eCB anandamide (AEA), throughout multiple corticolimbic brain regions.	aea	153-156	fatty-acid amide hydrolase-like	Rattus norvegicus	109-113
33452437-9	2021	This elevation of FAAH activity was associated with broad reductions in the content of AEA, whose decline was driven by central corticotropin releasing factor type 1 receptor signaling.	aea	87-90	fatty-acid amide hydrolase-like	Rattus norvegicus	18-22
33452437-10	2021	Colitis-induced anxiety was reversed following acute central inhibition of FAAH, suggesting that the reductions in AEA produced by colitis contributed to the generation of anxiety.	aea	115-118	fatty-acid amide hydrolase-like	Rattus norvegicus	75-79
33673103-1	2021	This study evaluated the effect of anandamide (AEA) on interleukin (IL)-1beta synthesis and gene expression of IL-1beta, its type I (IL-1R1) and II (IL-1R2) receptors, and IL-1 receptor antagonist (IL-1RN) in the hypothalamic structures, involved in the central control of reproduction, during inflammation.	aea	47-50	interleukin 1 alpha	Homo sapiens	55-77
33171147-10	2021	Taken together, our results show that the panicolytic consequences of the AEA enhancement in the SNpr are signalled by CB1R, suggesting that CB1R localised in axon terminals of CPu GABAergic neurons in the SNpr modulates the activity of the nigrotectal GABAergic pathway during the expression of defensive behaviours in threatening situations.	aea	74-77	cannabinoid receptor 1 (brain)	Mus musculus	119-123
33171147-10	2021	Taken together, our results show that the panicolytic consequences of the AEA enhancement in the SNpr are signalled by CB1R, suggesting that CB1R localised in axon terminals of CPu GABAergic neurons in the SNpr modulates the activity of the nigrotectal GABAergic pathway during the expression of defensive behaviours in threatening situations.	aea	74-77	cannabinoid receptor 1 (brain)	Mus musculus	141-145
33388673-12	2021	CONCLUSIONS: Our results suggest protective properties of nf-AEA, both peripherally and centrally, through a signaling pathway that would involve the type I angiotensin II receptor, Wilms tumor transcription factor 1, Hsp70, and iNOS.	aea	61-64	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	218-223
33388673-12	2021	CONCLUSIONS: Our results suggest protective properties of nf-AEA, both peripherally and centrally, through a signaling pathway that would involve the type I angiotensin II receptor, Wilms tumor transcription factor 1, Hsp70, and iNOS.	aea	61-64	nitric oxide synthase 2	Rattus norvegicus	229-233
33833828-3	2021	Levels of the endocannabinoid anandamide (AEA) seem to affect these depression-by-stress-related features and could be modulated by fatty acid amide hydrolase (FAAH).	aea	42-45	fatty acid amide hydrolase	Mus musculus	143-158
33833828-3	2021	Levels of the endocannabinoid anandamide (AEA) seem to affect these depression-by-stress-related features and could be modulated by fatty acid amide hydrolase (FAAH).	aea	42-45	fatty acid amide hydrolase	Mus musculus	160-164
33723207-4	2021	So far, one prominent target was inhibition of fatty acid amino hydrolase (FAAH), the degrading enzyme of the endocannabinoid anandamide (AEA).	aea	138-141	fatty acid amide hydrolase	Homo sapiens	47-73
33723207-4	2021	So far, one prominent target was inhibition of fatty acid amino hydrolase (FAAH), the degrading enzyme of the endocannabinoid anandamide (AEA).	aea	138-141	fatty acid amide hydrolase	Homo sapiens	75-79
33723207-5	2021	Research in humans remains scarce, but genetic studies have found that the single-nucleotide polymorphism (SNP) FAAH C385A (rs324420) is associated with lower catabolic performance of FAAH and increased levels of AEA.	aea	213-216	fatty acid amide hydrolase	Homo sapiens	112-116
33673103-6	2021	AEA injection (p < 0.05) suppressed LPS-induced expression of IL-1beta protein in the hypothalamus.	aea	0-3	interleukin 1 alpha	Homo sapiens	62-70
33673103-7	2021	The gene expression of IL-1beta, IL-1RN, and IL-1R2 in the hypothalamic structures was higher (p < 0.05) in animals treated with both LPS and AEA in comparison to other experimental groups.	aea	142-145	interleukin 1 alpha	Homo sapiens	23-31
33673103-7	2021	The gene expression of IL-1beta, IL-1RN, and IL-1R2 in the hypothalamic structures was higher (p < 0.05) in animals treated with both LPS and AEA in comparison to other experimental groups.	aea	142-145	interleukin 1 receptor antagonist	Homo sapiens	33-39
33673103-7	2021	The gene expression of IL-1beta, IL-1RN, and IL-1R2 in the hypothalamic structures was higher (p < 0.05) in animals treated with both LPS and AEA in comparison to other experimental groups.	aea	142-145	interleukin 1 receptor type 2	Homo sapiens	45-51
33673103-9	2021	Our study shows that AEA suppressed IL-1beta synthesis in the hypothalamus, likely affecting posttranscriptional levels of this cytokine synthesis.	aea	21-24	interleukin 1 alpha	Homo sapiens	36-44
33673103-10	2021	However, anti-inflammatory effect of AEA might also result from its stimulating action on IL-1RN and IL-1R2 gene expression.	aea	37-40	interleukin 1 receptor antagonist	Homo sapiens	90-96
33673103-10	2021	However, anti-inflammatory effect of AEA might also result from its stimulating action on IL-1RN and IL-1R2 gene expression.	aea	37-40	interleukin 1 receptor type 2	Homo sapiens	101-107
33314038-8	2021	Increased AEA signalling at vanilloid TRPV1 receptors impaired fear memory extinction.	aea	10-13	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	38-43
33490317-2	2021	In this study, we compared the effects of the pharmacological inhibition of the two major endocannabinoid-degrading enzymes [fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) for AEA and 2-AG, respectively] on stress-coping [forced swim test (FST) and tail suspension test (TST)] and anxiety-like [elevated-plus maze (EPM) and light-dark test (LDT)] behaviors in wild-type and FAAH knockout mice.	aea	198-201	fatty acid amide hydrolase	Mus musculus	125-151
33490317-2	2021	In this study, we compared the effects of the pharmacological inhibition of the two major endocannabinoid-degrading enzymes [fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) for AEA and 2-AG, respectively] on stress-coping [forced swim test (FST) and tail suspension test (TST)] and anxiety-like [elevated-plus maze (EPM) and light-dark test (LDT)] behaviors in wild-type and FAAH knockout mice.	aea	198-201	fatty acid amide hydrolase	Mus musculus	153-157
33490317-2	2021	In this study, we compared the effects of the pharmacological inhibition of the two major endocannabinoid-degrading enzymes [fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) for AEA and 2-AG, respectively] on stress-coping [forced swim test (FST) and tail suspension test (TST)] and anxiety-like [elevated-plus maze (EPM) and light-dark test (LDT)] behaviors in wild-type and FAAH knockout mice.	aea	198-201	monoglyceride lipase	Mus musculus	163-186
33490317-2	2021	In this study, we compared the effects of the pharmacological inhibition of the two major endocannabinoid-degrading enzymes [fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) for AEA and 2-AG, respectively] on stress-coping [forced swim test (FST) and tail suspension test (TST)] and anxiety-like [elevated-plus maze (EPM) and light-dark test (LDT)] behaviors in wild-type and FAAH knockout mice.	aea	198-201	monoglyceride lipase	Mus musculus	188-192
33459498-10	2021	Both substances significantly increased the release of insulin-like growth factor-1 and hepatocyte growth factor, while only AEA enhanced transforming growth factor-beta secretion.	aea	125-128	tumor necrosis factor	Homo sapiens	138-169
32860981-1	2020	Fatty acid amide hydrolase (FAAH) exerts its main function in the catabolism of the endogenous chemical messenger anandamide (AEA), thus modulating the endocannabinoid (eCB) pathway.	aea	126-129	fatty acid amide hydrolase	Mus musculus	0-26
33362550-1	2020	Classically, the endocannabinoid system (ECS) consists of endogenous lipids, of which the best known are anandamide (AEA) and 2 arachidonoylglycerol (2-AG), their enzyme machinery for synthesis and degradation and their specific receptors, cannabinoid receptor one (CB1) and cannabinoid receptor two (CB2).	aea	117-120	cannabinoid receptor 1	Homo sapiens	266-269
33362550-1	2020	Classically, the endocannabinoid system (ECS) consists of endogenous lipids, of which the best known are anandamide (AEA) and 2 arachidonoylglycerol (2-AG), their enzyme machinery for synthesis and degradation and their specific receptors, cannabinoid receptor one (CB1) and cannabinoid receptor two (CB2).	aea	117-120	cannabinoid receptor 2	Homo sapiens	301-304
33374180-2	2020	Fatty acid amide hydrolase (FAAH) is a membrane-bound enzyme principally responsible for the degradation of AEA, and thus it represents a relevant target to increase signaling thereof.	aea	108-111	fatty acid amide hydrolase	Homo sapiens	0-26
33374180-2	2020	Fatty acid amide hydrolase (FAAH) is a membrane-bound enzyme principally responsible for the degradation of AEA, and thus it represents a relevant target to increase signaling thereof.	aea	108-111	fatty acid amide hydrolase	Homo sapiens	28-32
33376801-10	2020	Capsaicin and anandamide (AEA) activated TRPV1 receptors with an EC50 of 61 nM and 4.3 muM, respectively, but TRPV1 showed no response to Delta9-THC, cannabidiol, and other minor cannabinoids.	aea	26-29	transient receptor potential cation channel subfamily V member 1	Homo sapiens	41-46
32860981-1	2020	Fatty acid amide hydrolase (FAAH) exerts its main function in the catabolism of the endogenous chemical messenger anandamide (AEA), thus modulating the endocannabinoid (eCB) pathway.	aea	126-129	fatty acid amide hydrolase	Mus musculus	28-32
32860981-5	2020	Herein, we have identified a new FAAH inhibitor (1-((1-methyl-1H-indol-2-yl)methyl)piperidin-4-yl)(oxazol-2-yl)methanone (8) which inhibits the hydrolysis of AEA in the brain with high potency (IC50 value 11 nM at a substrate concentration of 0.5 microM), and without showing time-dependency.	aea	158-161	fatty acid amide hydrolase	Mus musculus	33-37
32860939-4	2020	In this study, we investigated whether circulating AEA and 2-AG were modified by treatment with IFN-alpha and whether they were involved in the development of IFN-alpha-induced depression.	aea	51-54	interferon alpha 1	Homo sapiens	96-105
32860939-10	2020	We found a different pattern of change in peripheral AEA and 2-AG during and after IFN-alpha treatment.	aea	53-56	interferon alpha 1	Homo sapiens	83-92
32860939-13	2020	Interestingly, AEA, but not 2-AG, was significantly, negatively correlated with interleukin (IL)-2 and IL-17a at six months follow-up.	aea	15-18	interleukin 2	Homo sapiens	80-98
32860939-13	2020	Interestingly, AEA, but not 2-AG, was significantly, negatively correlated with interleukin (IL)-2 and IL-17a at six months follow-up.	aea	15-18	interleukin 17A	Homo sapiens	103-109
32860939-15	2020	Our findings suggest that AEA and 2-AG are involved in different stages of immunoregulation following IFN-alpha treatment, where AEA might be involved in chronic inflammation.	aea	26-29	interferon alpha 1	Homo sapiens	102-111
33000188-2	2020	As the ligand of cannabinoid type 1 (CB1) and 2 (CB2) receptors, anandamide (AEA) exerts benign antioxidant activities.	aea	77-80	cannabinoid receptor 1	Rattus norvegicus	37-40
33000188-2	2020	As the ligand of cannabinoid type 1 (CB1) and 2 (CB2) receptors, anandamide (AEA) exerts benign antioxidant activities.	aea	77-80	cannabinoid receptor 2	Rattus norvegicus	49-52
32447096-3	2020	Also, AEA induces bovine sperm capacitation, through CB1 and TRPV1 receptors.	aea	6-9	TRPV1	Bos taurus	61-66
32681461-13	2020	FAAH activity was inhibited in a dose-dependent manner in all dose groups after single and multiple doses of ASP3652, paralleled by an increase in plasma levels of anandamide (AEA).	aea	176-179	fatty acid amide hydrolase	Homo sapiens	0-4
32447096-6	2020	Also, we studied the activity of fatty acid amide hydrolase (FAAH), the enzyme that degrades AEA.	aea	93-96	fatty-acid amide hydrolase 1	Bos taurus	33-59
32447096-6	2020	Also, we studied the activity of fatty acid amide hydrolase (FAAH), the enzyme that degrades AEA.	aea	93-96	fatty-acid amide hydrolase 1	Bos taurus	61-65
32793630-5	2020	The first endogenous ligand identified for TRPV1 was the endocannabinoid, anandamide (AEA).	aea	86-89	transient receptor potential cation channel subfamily V member 1	Homo sapiens	43-48
32793630-9	2020	These results suggest that AEA enters TRPV1 via a novel location between helices S1-S4 via the lipid bilayer.	aea	27-30	transient receptor potential cation channel subfamily V member 1	Homo sapiens	38-43
32292082-1	2020	Introduction: Fatty acid amide hydrolase (FAAH) is a membrane-bound enzyme, that inactivates endogenous signaling lipids of the fatty acid amide family, including the endocannabinoid anandamide (N-arachidonoylethanolamine, AEA).	aea	195-221	fatty acid amide hydrolase	Homo sapiens	14-40
32292082-1	2020	Introduction: Fatty acid amide hydrolase (FAAH) is a membrane-bound enzyme, that inactivates endogenous signaling lipids of the fatty acid amide family, including the endocannabinoid anandamide (N-arachidonoylethanolamine, AEA).	aea	195-221	fatty acid amide hydrolase	Homo sapiens	42-46
32292082-1	2020	Introduction: Fatty acid amide hydrolase (FAAH) is a membrane-bound enzyme, that inactivates endogenous signaling lipids of the fatty acid amide family, including the endocannabinoid anandamide (N-arachidonoylethanolamine, AEA).	aea	223-226	fatty acid amide hydrolase	Homo sapiens	14-40
32292082-1	2020	Introduction: Fatty acid amide hydrolase (FAAH) is a membrane-bound enzyme, that inactivates endogenous signaling lipids of the fatty acid amide family, including the endocannabinoid anandamide (N-arachidonoylethanolamine, AEA).	aea	223-226	fatty acid amide hydrolase	Homo sapiens	42-46
32101384-4	2020	In pharmacokinetic and pharmacodynamic studies, PKM-833 showed excellent brain penetration and good oral bioavailability, and elevated anandamide (AEA) concentrations in the rat brain.	aea	147-150	pyruvate kinase M1/2	Rattus norvegicus	48-51
32323032-4	2020	In response to combined stimulation with cytokines, IL-1beta and TNFalpha, the murine aorta released several endocannabinoids, with anandamide (AEA) levels being the most significantly increased.	aea	144-147	interleukin 1 alpha	Mus musculus	52-60
32323032-4	2020	In response to combined stimulation with cytokines, IL-1beta and TNFalpha, the murine aorta released several endocannabinoids, with anandamide (AEA) levels being the most significantly increased.	aea	144-147	tumor necrosis factor	Mus musculus	65-73
32323032-6	2020	As revealed by RNA-Seq analysis, the induction of a subset of 21 inflammatory target genes, including the important cytokine CCL2 was blocked by AEA.	aea	145-148	chemokine (C-C motif) ligand 2	Mus musculus	125-129
32323032-8	2020	In the presence of AEA, ATAC-Seq analysis and chromatin-immunoprecipitations revealed that CCL2 induction was blocked due to increased levels of H3K27me3 and a decrease of H3K27ac leading to compacted chromatin structure in the CCL2 promoter.	aea	19-22	chemokine (C-C motif) ligand 2	Mus musculus	91-95
32323032-8	2020	In the presence of AEA, ATAC-Seq analysis and chromatin-immunoprecipitations revealed that CCL2 induction was blocked due to increased levels of H3K27me3 and a decrease of H3K27ac leading to compacted chromatin structure in the CCL2 promoter.	aea	19-22	chemokine (C-C motif) ligand 2	Mus musculus	228-232
32416152-2	2020	Fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) are two main enzymes responsible for the metabolism of the endocannabinoids anandamide (AEA) and 2-arachydonoyl glycerol (2-AG), respectively.	aea	157-160	fatty acid amide hydrolase	Mus musculus	0-26
32416152-2	2020	Fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) are two main enzymes responsible for the metabolism of the endocannabinoids anandamide (AEA) and 2-arachydonoyl glycerol (2-AG), respectively.	aea	157-160	fatty acid amide hydrolase	Mus musculus	28-32
32416152-2	2020	Fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) are two main enzymes responsible for the metabolism of the endocannabinoids anandamide (AEA) and 2-arachydonoyl glycerol (2-AG), respectively.	aea	157-160	monoglyceride lipase	Mus musculus	38-61
32416152-2	2020	Fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) are two main enzymes responsible for the metabolism of the endocannabinoids anandamide (AEA) and 2-arachydonoyl glycerol (2-AG), respectively.	aea	157-160	monoglyceride lipase	Mus musculus	63-67
32316539-4	2020	It was demonstrated that AEA inhibited GnRH stimulated luteinizing hormone (LH) and follicle stimulating hormone (FSH) secretion from the AP explants.	aea	25-28	gonadotropin releasing hormone 1	Homo sapiens	39-43
32316539-6	2020	AEA also affected gonadoliberin receptor (GnRHR) synthesis and expression.	aea	0-3	gonadotropin releasing hormone receptor	Homo sapiens	42-47
31629892-1	2020	BACKGROUND: Fatty-acid amide hydrolase (FAAH) is an intracellular serine hydrolase that catalyzes the cleavage of endogenous fatty-acid amides, including the endocannabinoid anandamide (AEA).	aea	186-189	fatty-acid amide hydrolase-like	Rattus norvegicus	12-38
31816339-1	2020	BIA 10-2474 (3-(1-(cyclohexyl(methyl)carbamoyl)-1H-imidazol-4-yl)pyridine 1-oxide) is a novel fatty acid amide hydrolase (FAAH) inhibitor developed by BIAL for the treatment of medical conditions which would benefit from enhanced levels of endogenous anandamide (AEA) such as pain disorders.	aea	263-266	fatty-acid amide hydrolase 1	Macaca fascicularis	94-120
31816339-1	2020	BIA 10-2474 (3-(1-(cyclohexyl(methyl)carbamoyl)-1H-imidazol-4-yl)pyridine 1-oxide) is a novel fatty acid amide hydrolase (FAAH) inhibitor developed by BIAL for the treatment of medical conditions which would benefit from enhanced levels of endogenous anandamide (AEA) such as pain disorders.	aea	263-266	fatty-acid amide hydrolase 1	Macaca fascicularis	122-126
31923023-9	2020	Our results show that the chronic administration of AEA and sucralose intake induces an overexpression of DeltaFosB in the infralimbic cortex (Cx), nucleus accumbens (NAc) core, shell, and central nucleus of amygdala (Amy).	aea	52-55	FosB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	106-115
31923023-10	2020	These results suggest that the possible interaction between receptors CB1 and T1R3 has consequences not only in taste perception but also that AEA intervenes in the activity of dopaminergic nuclei such as the NAc, and that the chronic administration AEA and sucralose intake induce long-term changes in the reward system.	aea	143-146	taste 1 receptor member 3	Homo sapiens	78-82
31923023-10	2020	These results suggest that the possible interaction between receptors CB1 and T1R3 has consequences not only in taste perception but also that AEA intervenes in the activity of dopaminergic nuclei such as the NAc, and that the chronic administration AEA and sucralose intake induce long-term changes in the reward system.	aea	250-253	cannabinoid receptor 1	Homo sapiens	70-73
31923023-10	2020	These results suggest that the possible interaction between receptors CB1 and T1R3 has consequences not only in taste perception but also that AEA intervenes in the activity of dopaminergic nuclei such as the NAc, and that the chronic administration AEA and sucralose intake induce long-term changes in the reward system.	aea	250-253	taste 1 receptor member 3	Homo sapiens	78-82
31935683-6	2020	They demonstrated the stable encapsulation of AEA in Nps-AEA/PCL, as well as its dose-dependent capacity to induce the expression of iNOS and NO levels and to decrease the Na+/K+ ATPase activity in HK2 cells.	aea	46-49	nitric oxide synthase 2	Homo sapiens	133-137
31935683-6	2020	They demonstrated the stable encapsulation of AEA in Nps-AEA/PCL, as well as its dose-dependent capacity to induce the expression of iNOS and NO levels and to decrease the Na+/K+ ATPase activity in HK2 cells.	aea	46-49	hexokinase 2	Homo sapiens	198-201
31935683-7	2020	Obtaining Nps-AEA/PCL by electrospraying would represent a promising methodology for a novel AEA pharmaceutical formulation development with optimal physicochemical properties, physical stability and biological activity on HK2 cells.	aea	14-17	hexokinase 2	Homo sapiens	223-226
31948828-1	2020	Pharmacological inhibition of the enzyme fatty acid amide hydrolase (FAAH), which terminates signaling of the endocannabinoid N-arachidonoylethanolamine (or anandamide, AEA), exerts favourable effects in rodent models of stress-related depression.	aea	126-152	fatty-acid amide hydrolase-like	Rattus norvegicus	69-73
32041998-1	2020	Fatty acid amide hydrolase (FAAH) is a membrane-bound homodimeric enzyme that in vivo controls content and biological activity of N-arachidonoylethanolamine (AEA) and other relevant bioactive lipids termed endocannabinoids.	aea	130-156	fatty acid amide hydrolase	Homo sapiens	28-32
32041998-1	2020	Fatty acid amide hydrolase (FAAH) is a membrane-bound homodimeric enzyme that in vivo controls content and biological activity of N-arachidonoylethanolamine (AEA) and other relevant bioactive lipids termed endocannabinoids.	aea	158-161	fatty acid amide hydrolase	Homo sapiens	28-32
32041998-6	2020	Kinetic analysis of AEA hydrolysis by rat FAAH and its F432A mutant demonstrated a Hill coefficient of ~1.6, that instead was ~1.0 in the W445Y mutant.	aea	20-23	fatty-acid amide hydrolase-like	Rattus norvegicus	42-46
32041998-7	2020	Of note, also human FAAH catalysed an allosteric hydrolysis of AEA, showing a Hill coefficient of ~1.9.	aea	63-66	fatty acid amide hydrolase	Homo sapiens	20-24
31629892-1	2020	BACKGROUND: Fatty-acid amide hydrolase (FAAH) is an intracellular serine hydrolase that catalyzes the cleavage of endogenous fatty-acid amides, including the endocannabinoid anandamide (AEA).	aea	186-189	fatty-acid amide hydrolase-like	Rattus norvegicus	40-44
31629892-2	2020	We previously reported that the peripherally restricted FAAH inhibitor URB937, which selectively increases AEA levels outside the central nervous system, reduces hyperalgesia and c-Fos expression in the trigeminal nucleus caudalis (TNC) and the locus coeruleus in an animal model of migraine based on nitroglycerin (NTG) administration.	aea	107-110	fatty-acid amide hydrolase-like	Rattus norvegicus	56-60
31141804-1	2020	The endocannabinoids (ECs) N-arachidonylethanolamide (anandamide; AEA) and 2-arachidonoylglycerol (2-AG) participate in the control of feed intake and energy metabolism.	aea	66-69	Feed intake	Bos taurus	135-146
31843894-7	2020	Since stress-induced activation of fatty acid amide hydrolase (FAAH) reduces AEA, we confirmed that oral administration of an FAAH inhibitor during stress prevents the increase in synaptic excitation in the BLA soon after stress.	aea	77-80	fatty-acid amide hydrolase-like	Rattus norvegicus	35-61
31843894-7	2020	Since stress-induced activation of fatty acid amide hydrolase (FAAH) reduces AEA, we confirmed that oral administration of an FAAH inhibitor during stress prevents the increase in synaptic excitation in the BLA soon after stress.	aea	77-80	fatty-acid amide hydrolase-like	Rattus norvegicus	63-67
31843894-7	2020	Since stress-induced activation of fatty acid amide hydrolase (FAAH) reduces AEA, we confirmed that oral administration of an FAAH inhibitor during stress prevents the increase in synaptic excitation in the BLA soon after stress.	aea	77-80	fatty-acid amide hydrolase-like	Rattus norvegicus	126-130
31141804-9	2020	The results show a potential involvement of AEA in stimulating feed intake and of 2-AG in regulating energy metabolism of early lactating cows.	aea	44-47	Feed intake	Bos taurus	63-74
32580926-9	2020	Leptin, insulin, BMI, WC, and BF% were significant independent predictors of AEA and 2-AG in the hierarchical regression model (P<.001) and explained 65% and 68% of variance in AEA and 2-AG respectively (P<0.001).	aea	177-180	leptin	Homo sapiens	0-6
32580926-10	2020	CONCLUSION: The findings showed that levels of AEA and 2-AG were associated with BMI, WC, BF%, and leptin and insulin levels.	aea	47-50	leptin	Homo sapiens	99-105
32580926-2	2020	The present study was carried out to investigate AEA and 2-AG levels and their association with leptin, insulin, orexin - A, and anthropometric indices in obese women.	aea	49-52	leptin	Homo sapiens	96-102
32580926-10	2020	CONCLUSION: The findings showed that levels of AEA and 2-AG were associated with BMI, WC, BF%, and leptin and insulin levels.	aea	47-50	insulin	Homo sapiens	110-117
32580926-6	2020	RESULTS: Significant correlations were revealed between AEA and 2-AG with leptin, BMI, waist circumference (WC) and body fat percent (BF%) (P<0.001).	aea	56-59	leptin	Homo sapiens	74-80
32580926-11	2020	Also, BMI, WC, BF%, leptin and, insulin levels can have predictive value for determining AEA and 2-AG.	aea	89-92	leptin	Homo sapiens	20-26
32580926-9	2020	Leptin, insulin, BMI, WC, and BF% were significant independent predictors of AEA and 2-AG in the hierarchical regression model (P<.001) and explained 65% and 68% of variance in AEA and 2-AG respectively (P<0.001).	aea	77-80	leptin	Homo sapiens	0-6
32580926-11	2020	Also, BMI, WC, BF%, leptin and, insulin levels can have predictive value for determining AEA and 2-AG.	aea	89-92	insulin	Homo sapiens	32-39
31629610-2	2019	FAAH is an enzyme implicated in the hydrolysis of the endocannabinoid N-arachidonoylethanolamine (AEA), which is a partial agonist of the CB1 receptor.	aea	70-96	fatty-acid amide hydrolase-like	Rattus norvegicus	0-4
31629610-2	2019	FAAH is an enzyme implicated in the hydrolysis of the endocannabinoid N-arachidonoylethanolamine (AEA), which is a partial agonist of the CB1 receptor.	aea	98-101	fatty-acid amide hydrolase-like	Rattus norvegicus	0-4
31484847-1	2019	Anandamide (AEA) played potent neuroprotective activities via cannabinoid type 1 (CB1) and 2 (CB2) receptor.	aea	12-15	cannabinoid receptor 1 (brain)	Mus musculus	62-92
30421483-4	2019	In both genotypes, EtOH treatment caused no changes in baseline endocannabinoid levels, although FAAH KO mice displayed higher baseline N-arachidonoylethanolamine levels than WT mice.	aea	136-162	fatty acid amide hydrolase	Mus musculus	97-101
30532004-2	2019	The major AEA degrading enzyme is fatty acid amide hydrolase (FAAH).	aea	10-13	fatty acid amide hydrolase	Homo sapiens	34-60
31487817-4	2019	Knocking down COXs, particularly COX-1, significantly reduced the release of PGs from muscle cells, especially PGE2 and PGF2alpha, as well as oleoylethanolamide (OEA) and arachidonoylethanolamine (AEA).	aea	197-200	cytochrome c oxidase I, mitochondrial	Mus musculus	33-38
30822695-3	2019	Fatty acid amide hydrolase (FAAH) is the major enzyme that degrades the endocannabinoid arachidonoylethanolamine (AEA), an important regulator of inflammation, and its downstream metabolites such as arachidonic acid (AA) are also involved in inflammation.	aea	114-117	fatty-acid amide hydrolase 1	Oryctolagus cuniculus	0-26
30822695-3	2019	Fatty acid amide hydrolase (FAAH) is the major enzyme that degrades the endocannabinoid arachidonoylethanolamine (AEA), an important regulator of inflammation, and its downstream metabolites such as arachidonic acid (AA) are also involved in inflammation.	aea	114-117	fatty-acid amide hydrolase 1	Oryctolagus cuniculus	28-32
30822695-12	2019	The FAAH inhibitor URB937 administered not before but 2.5 h after OLV attenuated OLV-induced lung injury by increasing AEA levels and reducing the levels of downstream metabolites including AA, PGI2, TXA2, and LTB4.	aea	119-122	fatty acid amide hydrolase	Homo sapiens	4-8
30822695-13	2019	CONCLUSIONS: Posttreatment with the FAAH inhibitor URB937 attenuated OLV-induced lung injury in rabbits and was associated with increased AEA levels and decreased levels of AA and its downstream metabolites.	aea	138-141	fatty-acid amide hydrolase 1	Oryctolagus cuniculus	36-40
30532004-2	2019	The major AEA degrading enzyme is fatty acid amide hydrolase (FAAH).	aea	10-13	fatty acid amide hydrolase	Homo sapiens	62-66
30532004-6	2019	This approach led to specific FAAH overexpression at the postsynaptic site of CA1-CA3 neurons, to increased FAAH enzymatic activity, and, in consequence, to decreased hippocampal levels of AEA and palmitoylethanolamide (PEA), but the levels of the second major endocannabinoid 2-arachidonoyl glycerol (2-AG) and of oleoylethanolamide (OEA) were unchanged.	aea	189-192	fatty acid amide hydrolase	Mus musculus	30-34
30532004-6	2019	This approach led to specific FAAH overexpression at the postsynaptic site of CA1-CA3 neurons, to increased FAAH enzymatic activity, and, in consequence, to decreased hippocampal levels of AEA and palmitoylethanolamide (PEA), but the levels of the second major endocannabinoid 2-arachidonoyl glycerol (2-AG) and of oleoylethanolamide (OEA) were unchanged.	aea	189-192	carbonic anhydrase 1	Mus musculus	78-81
30532004-6	2019	This approach led to specific FAAH overexpression at the postsynaptic site of CA1-CA3 neurons, to increased FAAH enzymatic activity, and, in consequence, to decreased hippocampal levels of AEA and palmitoylethanolamide (PEA), but the levels of the second major endocannabinoid 2-arachidonoyl glycerol (2-AG) and of oleoylethanolamide (OEA) were unchanged.	aea	189-192	carbonic anhydrase 3	Mus musculus	82-85
31110238-8	2019	Finally, AEA uptake by PC3 prostate cancer and SH-SY5Y neuroblastoma cells, which express functional Panx1 channels, was not inhibited by carbenoxolone.	aea	9-12	pannexin 1	Homo sapiens	101-106
31117309-2	2019	Inhibition of FAAH increases endogenous levels of fatty acid ethanolamides such as anandamide (AEA) and thus consitutes an indirect strategy that can be used to modulate endocannabinoid tone.	aea	95-98	fatty acid amide hydrolase	Homo sapiens	14-18
31110238-1	2019	The large pore ion channel pannexin-1 (Panx1) has been reported to play a role in the cellular uptake and release of anandamide (AEA) in the hippocampus.	aea	129-132	pannexin 1	Homo sapiens	27-37
28104279-2	2019	The endocannabinoid system is known to modulate the nigrostriatal pathway through endogenous ligands such as anandamide (AEA), which is hydrolysed by fatty acid amide hydrolase (FAAH).	aea	121-124	fatty acid amide hydrolase	Mus musculus	161-176
31110238-1	2019	The large pore ion channel pannexin-1 (Panx1) has been reported to play a role in the cellular uptake and release of anandamide (AEA) in the hippocampus.	aea	129-132	pannexin 1	Homo sapiens	39-44
28104279-2	2019	The endocannabinoid system is known to modulate the nigrostriatal pathway through endogenous ligands such as anandamide (AEA), which is hydrolysed by fatty acid amide hydrolase (FAAH).	aea	121-124	fatty acid amide hydrolase	Mus musculus	178-182
30739035-2	2019	Inhibition of fatty-acid amide hydrolase (FAAH), the major enzyme catalyzing the degradation of anandamide (AEA), an endocannabinoid, and other fatty-acid amides, suppresses pain without unwanted side effects typical of direct CB1 agonists.	aea	108-111	fatty acid amide hydrolase	Homo sapiens	14-40
30739035-2	2019	Inhibition of fatty-acid amide hydrolase (FAAH), the major enzyme catalyzing the degradation of anandamide (AEA), an endocannabinoid, and other fatty-acid amides, suppresses pain without unwanted side effects typical of direct CB1 agonists.	aea	108-111	fatty acid amide hydrolase	Homo sapiens	42-46
30739035-2	2019	Inhibition of fatty-acid amide hydrolase (FAAH), the major enzyme catalyzing the degradation of anandamide (AEA), an endocannabinoid, and other fatty-acid amides, suppresses pain without unwanted side effects typical of direct CB1 agonists.	aea	108-111	cannabinoid receptor 1	Homo sapiens	227-230
30504766-6	2018	Adipocyte OGT stimulates hyperphagia by transcriptional activation of de novo lipid desaturation and accumulation of N-arachidonyl ethanolamine (AEA), an endogenous appetite-inducing cannabinoid (CB).	aea	145-148	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	10-13
30842391-6	2019	RESULTS FAAH expression was significantly lower in fibroids, resulting in a NAPE-PLD: FAAH ratio that favors higher AEA levels in pre-menopausal tissues, whilst PEA levels were significantly lower, particularly in post-menopausal women, suggesting PEA protects against fibroid pathogenesis.	aea	116-119	fatty acid amide hydrolase	Homo sapiens	8-12
30842391-6	2019	RESULTS FAAH expression was significantly lower in fibroids, resulting in a NAPE-PLD: FAAH ratio that favors higher AEA levels in pre-menopausal tissues, whilst PEA levels were significantly lower, particularly in post-menopausal women, suggesting PEA protects against fibroid pathogenesis.	aea	116-119	N-acyl phosphatidylethanolamine phospholipase D	Homo sapiens	76-84
30842391-6	2019	RESULTS FAAH expression was significantly lower in fibroids, resulting in a NAPE-PLD: FAAH ratio that favors higher AEA levels in pre-menopausal tissues, whilst PEA levels were significantly lower, particularly in post-menopausal women, suggesting PEA protects against fibroid pathogenesis.	aea	116-119	fatty acid amide hydrolase	Homo sapiens	86-90
30573646-1	2019	Increased anandamide (AEA) signaling through inhibition of its catabolic enzyme fatty acid amide hydrolase (FAAH) in the basolateral complex of amygdala (BLA) is thought to buffer against the effects of stress and reduces behavioral signs of anxiety and fear.	aea	22-25	fatty-acid amide hydrolase-like	Rattus norvegicus	80-106
30573646-1	2019	Increased anandamide (AEA) signaling through inhibition of its catabolic enzyme fatty acid amide hydrolase (FAAH) in the basolateral complex of amygdala (BLA) is thought to buffer against the effects of stress and reduces behavioral signs of anxiety and fear.	aea	22-25	fatty-acid amide hydrolase-like	Rattus norvegicus	108-112
30784807-8	2019	With activation of TRPV1 using AEA also, PSM was significantly (P &lt; 0.05) decreased till 1h and thereafter the PSM was sustained to the level as observed in control.	aea	31-34	transient receptor potential cation channel subfamily V member 1	Homo sapiens	19-24
30659320-5	2019	We demonstrate that THC (10-40 microM) impairs placental endocannabinoid system by disrupting the endocannabinoid anandamide (AEA) levels and the expression of AEA synthetic and degrading enzymes N-arachidonoylphosphatidylethanolamine-specific phospholipase D (NAPE-PLD) and fatty acid amide hydrolase (FAAH), respectively.	aea	160-163	N-acyl phosphatidylethanolamine phospholipase D	Homo sapiens	196-259
30126012-1	2018	BACKGROUND AND OBJECTIVES: The endogenous cannabinoid anandamide (AEA), an agonist at type-1 cannabinoid (CB1) receptors, is metabolized by fatty acid amide hydrolase (FAAH).	aea	66-69	cannabinoid receptor 1	Homo sapiens	106-109
29071769-1	2018	Fatty acid amide hydrolase (FAAH) is an enzyme that prominently degrades the major endocannabinoid N-arachidonoylethanolamine (anandamide).	aea	99-125	fatty-acid amide hydrolase-like	Rattus norvegicus	28-32
29071769-1	2018	Fatty acid amide hydrolase (FAAH) is an enzyme that prominently degrades the major endocannabinoid N-arachidonoylethanolamine (anandamide).	aea	127-137	fatty-acid amide hydrolase-like	Rattus norvegicus	28-32
30126012-1	2018	BACKGROUND AND OBJECTIVES: The endogenous cannabinoid anandamide (AEA), an agonist at type-1 cannabinoid (CB1) receptors, is metabolized by fatty acid amide hydrolase (FAAH).	aea	66-69	fatty acid amide hydrolase	Homo sapiens	168-172
30114402-4	2018	A major endocannabinoid, anandamide (N-arachidonoylethanolamine, AEA), is metabolized by fatty acid amide hydrolase (FAAH).	aea	37-63	fatty acid amide hydrolase	Homo sapiens	117-121
30460698-2	2018	We found that AEA stimulates and activates AMPKalpha through a Ca2+ -dependent/Calmodulin (CaM)-dependent pathway as the specific inhibitor of the Ca2+ /Calmodulin kinase kinase beta (CaMKKbeta) STO-609 abolishes the AMPK phosphorylation/activation.	aea	14-17	calcium/calmodulin dependent protein kinase kinase 2	Homo sapiens	184-193
30460698-2	2018	We found that AEA stimulates and activates AMPKalpha through a Ca2+ -dependent/Calmodulin (CaM)-dependent pathway as the specific inhibitor of the Ca2+ /Calmodulin kinase kinase beta (CaMKKbeta) STO-609 abolishes the AMPK phosphorylation/activation.	aea	14-17	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	43-47
30460698-10	2018	In conclusion, we show that the CaMKKbeta/AMPKalpha pathway, downstream of the PI3K/AKT pathway, is activated by AEA in human platelets and leads to increase NO levels producing beneficial effects during ischemic conditions and contributing to extend platelet survival.	aea	113-116	AKT serine/threonine kinase 1	Homo sapiens	84-87
30460698-7	2018	We have demonstrated that AEA stimulates VASP phosphorylation on both thr278 and ser239 that is strongly inhibited by STO-609, LY294002, and MK2206.	aea	26-29	vasodilator stimulated phosphoprotein	Homo sapiens	41-45
30460698-9	2018	SR144528, an antagonist of type 2 cannabinoid receptor (CB2), has a less-potent effect, suggesting that the CB1 receptor is overall involved in the AEA effect.	aea	148-151	cannabinoid receptor 2	Homo sapiens	56-59
30460698-9	2018	SR144528, an antagonist of type 2 cannabinoid receptor (CB2), has a less-potent effect, suggesting that the CB1 receptor is overall involved in the AEA effect.	aea	148-151	cannabinoid receptor 1	Homo sapiens	108-111
30460698-10	2018	In conclusion, we show that the CaMKKbeta/AMPKalpha pathway, downstream of the PI3K/AKT pathway, is activated by AEA in human platelets and leads to increase NO levels producing beneficial effects during ischemic conditions and contributing to extend platelet survival.	aea	113-116	calcium/calmodulin dependent protein kinase kinase 2	Homo sapiens	32-41
29388323-7	2018	Upon CB1 activation, N-oleoylethanolamide and N-palmitoylethanolamide, two AEA congeners that do not interact directly with cannabinoid receptors, were enhanced in the striatum.	aea	75-78	cannabinoid receptor 1 (brain)	Mus musculus	5-8
29977073-11	2018	Indeed, exposure to shock and SRs affected eCB content: increased 2-arachidonoyl-glycerol (2-AG) and N-arachidonylethanolamine (AEA) levels in the CA1, decreased serum and BLA AEA levels while shock exposure increased FAAH activity in the CA1 and BLA.	aea	128-131	carbonic anhydrase 1	Homo sapiens	147-150
29967158-4	2018	Therefore, we explored the interaction between leptin and endocannabinoid signaling with a focus on fatty acid amide hydrolase (FAAH), the primary degradative enzyme for the endocannabinoid N-arachidonoylethanolamine (anandamide; AEA).	aea	190-216	fatty acid amide hydrolase	Mus musculus	111-126
29967158-4	2018	Therefore, we explored the interaction between leptin and endocannabinoid signaling with a focus on fatty acid amide hydrolase (FAAH), the primary degradative enzyme for the endocannabinoid N-arachidonoylethanolamine (anandamide; AEA).	aea	190-216	fatty acid amide hydrolase	Mus musculus	128-132
29110674-2	2017	A number of endocannabinoids including N- arachidonoylethanolamide (anandamide, AEA) and 2-arachidonyl glycerol (2-AG) with activity at the cannabinoid receptors (CBR) CBR1 and CBR2, have been identified.	aea	68-78	carbonyl reductase [NADPH] 1	Canis lupus familiaris	168-172
28726298-8	2018	In contrast, the fatty acid amide hydrolase (FAAH) inhibitor URB597 increased levels of AEA and related N-acylethanolamines, an effect associated with the attenuation of TLR3-induced inflammatory responses in the hypothalamus, but not the spleen, of male and female rats.	aea	88-91	fatty-acid amide hydrolase-like	Rattus norvegicus	17-43
28726298-8	2018	In contrast, the fatty acid amide hydrolase (FAAH) inhibitor URB597 increased levels of AEA and related N-acylethanolamines, an effect associated with the attenuation of TLR3-induced inflammatory responses in the hypothalamus, but not the spleen, of male and female rats.	aea	88-91	fatty-acid amide hydrolase-like	Rattus norvegicus	45-49
30203570-1	2018	Liver fatty-acid-binding protein (FABP1, L-FABP) is the major cytosolic binding/chaperone protein for both precursor arachidonic acid (ARA) and the endocannabinoid (EC) products N-arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol (2-AG).	aea	178-204	fatty acid binding protein 1, liver	Mus musculus	34-39
30203570-1	2018	Liver fatty-acid-binding protein (FABP1, L-FABP) is the major cytosolic binding/chaperone protein for both precursor arachidonic acid (ARA) and the endocannabinoid (EC) products N-arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol (2-AG).	aea	178-204	fatty acid binding protein 1, liver	Mus musculus	41-47
30203570-1	2018	Liver fatty-acid-binding protein (FABP1, L-FABP) is the major cytosolic binding/chaperone protein for both precursor arachidonic acid (ARA) and the endocannabinoid (EC) products N-arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol (2-AG).	aea	206-209	fatty acid binding protein 1, liver	Mus musculus	34-39
30203570-1	2018	Liver fatty-acid-binding protein (FABP1, L-FABP) is the major cytosolic binding/chaperone protein for both precursor arachidonic acid (ARA) and the endocannabinoid (EC) products N-arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol (2-AG).	aea	206-209	fatty acid binding protein 1, liver	Mus musculus	41-47
30203570-3	2018	In vitro assays revealed that FABP1 considerably enhanced monoacylglycerol lipase hydrolysis of 2-AG but only modestly enhanced AEA hydrolysis by fatty-acid amide hydrolase.	aea	128-131	fatty acid binding protein 1, liver	Mus musculus	30-35
30203570-6	2018	FABP1 bound NBD-ARA with 2:1 stoichiometry analogous to ARA, but bound NBD-2-AG and NBD-AEA with 1:1 stoichiometry-apparently at different sites in FABP1"s binding cavity.	aea	88-91	fatty acid binding protein 1, liver	Mus musculus	0-5
30203570-9	2018	These data indicated that FABP1 impacts hepatocyte EC levels by binding EC and differentially impacts their intracellular hydrolysis (2-AG) and uptake (AEA).	aea	152-155	fatty acid binding protein 1, liver	Mus musculus	26-31
29519609-11	2018	One hour after the shock, N-arachidonoylethanolamine (AEA) was increased in the BLA and decreased in the CA1.	aea	26-52	carbonic anhydrase 1	Rattus norvegicus	105-108
29519609-11	2018	One hour after the shock, N-arachidonoylethanolamine (AEA) was increased in the BLA and decreased in the CA1.	aea	54-57	carbonic anhydrase 1	Rattus norvegicus	105-108
29288688-11	2018	Additionally these macamides, in a manner similar to the analogous endocannabinoid AEA, interact with other targets such as PPARgamma to regulate metabolism and energy homeostasis, cell differentiation and inflammation.	aea	83-86	peroxisome proliferator activated receptor gamma	Homo sapiens	124-133
29165386-2	2017	We have previously demonstrated that systemic administration of ghrelin antagonist (JMV2959) significantly decreased morphine-induced dopamine and anandamide (N-arachidonoylethanolamine, AEA) increase in the NACSh.	aea	159-185	ghrelin and obestatin prepropeptide	Rattus norvegicus	64-71
28770703-10	2017	The levels of AEA were correlated with the number of oral ulcer, ESR, and CRP.	aea	14-17	C-reactive protein	Homo sapiens	74-77
28770703-12	2017	CONCLUSIONS: Serum AEA was increased in BD patients and correlated with oral ulcer, ESR and CRP.	aea	19-22	C-reactive protein	Homo sapiens	92-95
28209423-3	2017	In the amygdala, acute stress activates the enzymatic clearance of the eCB N-arachidonoylethanolamine via fatty acid amide hydrolase (FAAH), although it is unclear whether chronic dysregulation of CRF systems induces maladaptive changes in amygdalar eCB signaling.	aea	75-101	fatty-acid amide hydrolase-like	Rattus norvegicus	134-138
29085337-8	2017	LIF production was promoted by low amount of AEA administration (1-10 muM), while the promotion was reduced by higher concentration of AEA (50 muM).	aea	45-48	LIF interleukin 6 family cytokine	Homo sapiens	0-3
29085337-8	2017	LIF production was promoted by low amount of AEA administration (1-10 muM), while the promotion was reduced by higher concentration of AEA (50 muM).	aea	45-48	latexin	Homo sapiens	70-73
29085337-8	2017	LIF production was promoted by low amount of AEA administration (1-10 muM), while the promotion was reduced by higher concentration of AEA (50 muM).	aea	135-138	LIF interleukin 6 family cytokine	Homo sapiens	0-3
29085337-8	2017	LIF production was promoted by low amount of AEA administration (1-10 muM), while the promotion was reduced by higher concentration of AEA (50 muM).	aea	135-138	latexin	Homo sapiens	143-146
29085337-9	2017	LIF levels were decreased by AM251 or AM630, compared with AEA alone.	aea	59-62	LIF interleukin 6 family cytokine	Homo sapiens	0-3
29085337-11	2017	Different concentrations of AEA could stimulate dynamic changes in LIF production.	aea	28-31	LIF interleukin 6 family cytokine	Homo sapiens	67-70
28625856-6	2017	Our aim was to investigate the effect of an endogenous cannabinoid, anandamide (AEA) on the NTG-induced changes on serotonin transporter (5-HTT) expression in the upper cervical spinal cord (C1-C2) of the rat, where most of the trigeminal nociceptive afferents convey.	aea	80-83	solute carrier family 6 member 4	Rattus norvegicus	115-136
28981653-6	2017	Results: Ileal expression of CB2R and the endocannabinoid anandamide [AEA] was increased in actively inflamed TNF ARE/+ mice compared with controls.	aea	70-73	tumor necrosis factor	Mus musculus	110-113
28209423-11	2017	CONCLUSIONS: Pathological anxiety and stress hypersensitivity are driven by constitutive increases in CRF1 signaling that dysregulate N-arachidonoylethanolamine signaling mechanisms and reduce neuronal inhibitory control of CeA glutamatergic synapses.	aea	134-160	corticotropin releasing hormone receptor 1	Rattus norvegicus	102-106
28673548-1	2017	Substantial challenges exist for investigating the cannabinoid receptor type 1 (CB1)-mediated discriminative stimulus effects of the endocannabinoids, 2-arachidonoylglycerol (2-AG) and N-arachidonoylethanolamine (anandamide; AEA), compared with exogenous CB1 receptor agonists, such as Delta9-tetrahydrocannabinol (THC) and the synthetic cannabinoid CP55,940.	aea	185-211	cannabinoid receptor 1 (brain)	Mus musculus	51-83
28673548-1	2017	Substantial challenges exist for investigating the cannabinoid receptor type 1 (CB1)-mediated discriminative stimulus effects of the endocannabinoids, 2-arachidonoylglycerol (2-AG) and N-arachidonoylethanolamine (anandamide; AEA), compared with exogenous CB1 receptor agonists, such as Delta9-tetrahydrocannabinol (THC) and the synthetic cannabinoid CP55,940.	aea	185-211	cannabinoid receptor 1 (brain)	Mus musculus	80-83
28820005-2	2017	FAAH and MAGL hydrolyze the endocannabinoids anandamide (AEA) and 2-arachidonylglycerol (2-AG), respectively.	aea	57-60	fatty-acid amide hydrolase-like	Rattus norvegicus	0-4
28910408-3	2017	Additionally, we have investigated whether cyclooxygenase-2 (COX-2) can regulate the uptake of AEA into cells.	aea	95-98	prostaglandin-endoperoxide synthase 2	Homo sapiens	43-59
28910408-3	2017	Additionally, we have investigated whether cyclooxygenase-2 (COX-2) can regulate the uptake of AEA into cells.	aea	95-98	prostaglandin-endoperoxide synthase 2	Homo sapiens	61-66
28910408-8	2017	AEA uptake in both DU145 and RAW264.7 cells was inhibited by FAAH inhibition, but not by COX-2 inhibition, even in RAW264.7 cells where the expression of this enzyme had greatly been induced by lipopolysaccharide + interferon gamma treatment.	aea	0-3	fatty acid amide hydrolase	Mus musculus	61-65
28910408-10	2017	The data demonstrate that in DU145 cells, TNFalpha treatment changes the relative expression of the enzymes involved in the hydrolytic and oxygenation catabolic pathways for AEA.	aea	174-177	tumor necrosis factor	Homo sapiens	42-50
28820005-2	2017	FAAH and MAGL hydrolyze the endocannabinoids anandamide (AEA) and 2-arachidonylglycerol (2-AG), respectively.	aea	57-60	monoglyceride lipase	Rattus norvegicus	9-13
28624572-7	2017	Exposure to shock and reminders resulted in attenuated levels of the endocannabinoid N-arachidonylethanolamine (AEA) in the NAc; the cannabinoid CB1/2 receptor agonist WIN55,212-2 (5microg/side) microinjected into the NAc facilitated extinction in shocked rats.	aea	112-115	cannabinoid receptor 1	Rattus norvegicus	145-150
28258202-3	2017	For example, N-arachidonoyl-ethanolamine and 2-arachidonoyl-glycerol can be metabolized by cyclooxygenase-2 into PG-ethanolamide (PG-EA) and PG-glycerol (PG-G), respectively.	aea	13-40	prostaglandin-endoperoxide synthase 2	Homo sapiens	91-107
28193523-1	2017	Recent studies have shown that inhibition of fatty acid amide hydrolase (FAAH), the major degradative enzyme of the endocannabinoid N-arachidonoylethanolamine (AEA), produced antidepressant behavioral responses, but its underlying mechanism is not clear.	aea	132-158	fatty acid amide hydrolase	Mus musculus	56-71
28193523-1	2017	Recent studies have shown that inhibition of fatty acid amide hydrolase (FAAH), the major degradative enzyme of the endocannabinoid N-arachidonoylethanolamine (AEA), produced antidepressant behavioral responses, but its underlying mechanism is not clear.	aea	132-158	fatty acid amide hydrolase	Mus musculus	73-77
28193523-1	2017	Recent studies have shown that inhibition of fatty acid amide hydrolase (FAAH), the major degradative enzyme of the endocannabinoid N-arachidonoylethanolamine (AEA), produced antidepressant behavioral responses, but its underlying mechanism is not clear.	aea	160-163	fatty acid amide hydrolase	Mus musculus	56-71
28193523-1	2017	Recent studies have shown that inhibition of fatty acid amide hydrolase (FAAH), the major degradative enzyme of the endocannabinoid N-arachidonoylethanolamine (AEA), produced antidepressant behavioral responses, but its underlying mechanism is not clear.	aea	160-163	fatty acid amide hydrolase	Mus musculus	73-77
28193523-2	2017	Here we find that a systemic administration of the FAAH inhibitor PF3845 or an intra-CA1 application of AEA elicits an in vivo long-term depression (LTD) at excitatory glutamatergic CA3-CA1 synapses of the hippocampus.	aea	104-107	carbonic anhydrase 1	Mus musculus	85-88
28193523-2	2017	Here we find that a systemic administration of the FAAH inhibitor PF3845 or an intra-CA1 application of AEA elicits an in vivo long-term depression (LTD) at excitatory glutamatergic CA3-CA1 synapses of the hippocampus.	aea	104-107	carbonic anhydrase 3	Mus musculus	182-189
28193523-3	2017	The PF3845- and/or AEA-elicited LTD are abolished by the LTD-blocking peptide Tat-GluR2.	aea	19-22	glutamate receptor, ionotropic, AMPA2 (alpha 2)	Mus musculus	82-87
28234213-3	2017	Inhibition of the fatty acid amide hydrolase (FAAH), the endocannabinoid N-arachidonoylethanolamine (AEA) degradative enzyme, produces anti-anxiety effects without substantial "unwanted effects" of cannabinoids, but its anti-anxiety mechanism is unclear.	aea	73-99	fatty acid amide hydrolase	Mus musculus	18-44
28234213-3	2017	Inhibition of the fatty acid amide hydrolase (FAAH), the endocannabinoid N-arachidonoylethanolamine (AEA) degradative enzyme, produces anti-anxiety effects without substantial "unwanted effects" of cannabinoids, but its anti-anxiety mechanism is unclear.	aea	73-99	fatty acid amide hydrolase	Mus musculus	46-50
28234213-3	2017	Inhibition of the fatty acid amide hydrolase (FAAH), the endocannabinoid N-arachidonoylethanolamine (AEA) degradative enzyme, produces anti-anxiety effects without substantial "unwanted effects" of cannabinoids, but its anti-anxiety mechanism is unclear.	aea	101-104	fatty acid amide hydrolase	Mus musculus	18-44
28234213-3	2017	Inhibition of the fatty acid amide hydrolase (FAAH), the endocannabinoid N-arachidonoylethanolamine (AEA) degradative enzyme, produces anti-anxiety effects without substantial "unwanted effects" of cannabinoids, but its anti-anxiety mechanism is unclear.	aea	101-104	fatty acid amide hydrolase	Mus musculus	46-50
28234213-10	2017	CONCLUSION: We propose that the rapid anti-anxiety effects of FAAH inhibition are due to AEA activation of astroglial CB1R and subsequent basolateral amygdala LTD in vivo.	aea	89-92	fatty acid amide hydrolase	Mus musculus	62-66
28234213-10	2017	CONCLUSION: We propose that the rapid anti-anxiety effects of FAAH inhibition are due to AEA activation of astroglial CB1R and subsequent basolateral amygdala LTD in vivo.	aea	89-92	cannabinoid receptor 1 (brain)	Mus musculus	118-122
29430557-7	2017	After chronic acrolein exposure, levels of all 6 N-acyl ethanolamines in the screening library, including the endogenous cannabinoid and TRPV1 agonist, N-arachidonoyl ethanolamine, were elevated in trigeminal tissue and in the cerebellum.	aea	152-179	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	137-142
27062913-10	2017	These results indicate that AEA modulates the pro-aversive effects of intra-VMHdm-bicuculline treatment, recruiting CB1 cannabinoid receptors and the TRPV1 channel is involved in the AM251-related potentiation of bicuculline effects on non-oriented escape behaviour.	aea	28-31	cannabinoid receptor 1	Homo sapiens	116-119
27062913-10	2017	These results indicate that AEA modulates the pro-aversive effects of intra-VMHdm-bicuculline treatment, recruiting CB1 cannabinoid receptors and the TRPV1 channel is involved in the AM251-related potentiation of bicuculline effects on non-oriented escape behaviour.	aea	28-31	transient receptor potential cation channel subfamily V member 1	Homo sapiens	150-155
28750817-6	2017	Using a fluorescent probe displacement assay, we found SCP-2 binds the eCBs, AEA (Ki=0.68+-0.05muM) and 2-AG (Ki=0.37+-0.02muM), with moderate affinity.	aea	77-80	sterol carrier protein 2	Homo sapiens	55-60
28373843-13	2017	The endocannabinoids AEA and 2-AG have antihyperalgesic activity, which is dependent on cannabinoid receptor and GPR55 activation.	aea	21-24	G protein-coupled receptor 55	Mus musculus	113-118
26642910-1	2017	Exposure to chlorpyrifos (CPF) during the late preweanling period in rats inhibits the endocannabinoid metabolizing enzymes fatty acid hydrolase (FAAH) and monoacylglycerol lipase (MAGL), resulting in accumulation of their respective substrates anandamide (AEA) and 2-arachidonylglycerol (2-AG).	aea	257-260	fatty-acid amide hydrolase-like	Rattus norvegicus	124-144
26642910-1	2017	Exposure to chlorpyrifos (CPF) during the late preweanling period in rats inhibits the endocannabinoid metabolizing enzymes fatty acid hydrolase (FAAH) and monoacylglycerol lipase (MAGL), resulting in accumulation of their respective substrates anandamide (AEA) and 2-arachidonylglycerol (2-AG).	aea	257-260	fatty-acid amide hydrolase-like	Rattus norvegicus	146-150
26642910-1	2017	Exposure to chlorpyrifos (CPF) during the late preweanling period in rats inhibits the endocannabinoid metabolizing enzymes fatty acid hydrolase (FAAH) and monoacylglycerol lipase (MAGL), resulting in accumulation of their respective substrates anandamide (AEA) and 2-arachidonylglycerol (2-AG).	aea	257-260	monoglyceride lipase	Rattus norvegicus	181-185
26642910-8	2017	AEA levels were significantly elevated in all three treatment groups as were palmitoylethanolamide and oleoylethanolamide, which are also substrates for FAAH.	aea	0-3	fatty-acid amide hydrolase-like	Rattus norvegicus	153-157
28261100-1	2017	The endogenous cannabinoid (endocannabinoid) system regulates a diverse array of physiological processes and unsurprisingly possesses considerable potential targets for the potential treatment of numerous disease states, including two receptors (i.e., CB1 and CB2 receptors) and enzymes regulating their endogenous ligands N-arachidonoylethanolamine (anandamide) and 2-arachidonyl glycerol (2-AG).	aea	323-349	cannabinoid receptor 1	Homo sapiens	252-255
28261100-1	2017	The endogenous cannabinoid (endocannabinoid) system regulates a diverse array of physiological processes and unsurprisingly possesses considerable potential targets for the potential treatment of numerous disease states, including two receptors (i.e., CB1 and CB2 receptors) and enzymes regulating their endogenous ligands N-arachidonoylethanolamine (anandamide) and 2-arachidonyl glycerol (2-AG).	aea	323-349	cannabinoid receptor 2	Homo sapiens	260-263
29131068-15	2017	In the AEA-exposed dam brain, however, there was a decrease in ETB receptor (p = 0.043) and an increase in CB1 receptor expression (p = 0.033).	aea	7-10	endothelin receptor type B	Rattus norvegicus	63-66
29131068-15	2017	In the AEA-exposed dam brain, however, there was a decrease in ETB receptor (p = 0.043) and an increase in CB1 receptor expression (p = 0.033).	aea	7-10	cannabinoid receptor 1	Rattus norvegicus	107-110
28808587-6	2017	Western blots showed a 72% increase in CB1R abundance in AEA-treated 21-day-old mice, without differences in adult mice.	aea	57-60	cannabinoid receptor 1 (brain)	Mus musculus	39-43
27465665-11	2016	In supernatants from degranulation experiments, increased levels of the endocannabinoid and putative GPR55 ligand anandamide (AEA) were found, suggesting its possible autocrine control of neutrophil activity.	aea	126-129	G protein-coupled receptor 55	Mus musculus	101-106
27790143-0	2016	A Personal Retrospective: Elevating Anandamide (AEA) by Targeting Fatty Acid Amide Hydrolase (FAAH) and the Fatty Acid Binding Proteins (FABPs).	aea	48-51	fatty acid amide hydrolase	Homo sapiens	94-98
27544303-6	2016	AEA treatment induced a significant improvement in the depressive-like behavior, which was reversed by the CB1 antagonist AM251, without affecting the hyperglycemia or weight gain.	aea	0-3	cannabinoid receptor 1	Rattus norvegicus	107-110
27544303-7	2016	AEA was also able to restore the elevated CB1 expression and also to elevate the reduced level of 5-HT in the HIP from DBT animals.	aea	0-3	cannabinoid receptor 1	Rattus norvegicus	42-45
27385208-9	2016	JZL184 also partially substituted in AEA-trained FAAH mice in the water maze, suggesting incomplete overlap in the stimulus effects of AEA and JZL184.	aea	37-40	fatty acid amide hydrolase	Mus musculus	49-53
27516570-9	2016	Both AEA and 2-AG are primarily agonists of the CB1 receptor and to a lower degree CB2 and TRPV1r eceptors, but 2-AG has stronger affinity for these receptors.	aea	5-8	cannabinoid receptor 1	Homo sapiens	48-51
27516570-9	2016	Both AEA and 2-AG are primarily agonists of the CB1 receptor and to a lower degree CB2 and TRPV1r eceptors, but 2-AG has stronger affinity for these receptors.	aea	5-8	cannabinoid receptor 2	Homo sapiens	83-86
27516570-9	2016	Both AEA and 2-AG are primarily agonists of the CB1 receptor and to a lower degree CB2 and TRPV1r eceptors, but 2-AG has stronger affinity for these receptors.	aea	5-8	transient receptor potential cation channel subfamily V member 1	Homo sapiens	91-96
27516570-12	2016	The main enzymes responsible for the hydrolysis of AEA and 2-AG are FAAH and MAGL, respectively.	aea	51-54	fatty acid amide hydrolase	Homo sapiens	68-72
27516570-12	2016	The main enzymes responsible for the hydrolysis of AEA and 2-AG are FAAH and MAGL, respectively.	aea	51-54	monoglyceride lipase	Homo sapiens	77-81
26821211-3	2016	We have recently found that the stress-related neuropeptide corticotropin-releasing hormone (CRH), acting through the CRH type 1 receptor (CRHR1), can reduce AEA content by increasing its hydrolysis by the enzyme fatty acid amide hydrolase (FAAH) as well as increase 2-AG contents.	aea	158-161	corticotropin releasing hormone	Rattus norvegicus	93-96
27109320-1	2016	BACKGROUND AND PURPOSE: The enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) hydrolyze endogenous cannabinoids (eCBs), N-arachidonoyl ethanolamine (AEA) and 2-arachidonoyl glycerol (2-AG), respectively.	aea	147-174	fatty acid amide hydrolase	Mus musculus	47-62
27109320-1	2016	BACKGROUND AND PURPOSE: The enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) hydrolyze endogenous cannabinoids (eCBs), N-arachidonoyl ethanolamine (AEA) and 2-arachidonoyl glycerol (2-AG), respectively.	aea	147-174	fatty acid amide hydrolase	Mus musculus	64-68
27109320-1	2016	BACKGROUND AND PURPOSE: The enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) hydrolyze endogenous cannabinoids (eCBs), N-arachidonoyl ethanolamine (AEA) and 2-arachidonoyl glycerol (2-AG), respectively.	aea	147-174	monoglyceride lipase	Mus musculus	74-97
27109320-1	2016	BACKGROUND AND PURPOSE: The enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) hydrolyze endogenous cannabinoids (eCBs), N-arachidonoyl ethanolamine (AEA) and 2-arachidonoyl glycerol (2-AG), respectively.	aea	147-174	monoglyceride lipase	Mus musculus	99-103
27109320-1	2016	BACKGROUND AND PURPOSE: The enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) hydrolyze endogenous cannabinoids (eCBs), N-arachidonoyl ethanolamine (AEA) and 2-arachidonoyl glycerol (2-AG), respectively.	aea	176-179	fatty acid amide hydrolase	Mus musculus	47-62
27109320-1	2016	BACKGROUND AND PURPOSE: The enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) hydrolyze endogenous cannabinoids (eCBs), N-arachidonoyl ethanolamine (AEA) and 2-arachidonoyl glycerol (2-AG), respectively.	aea	176-179	fatty acid amide hydrolase	Mus musculus	64-68
27109320-1	2016	BACKGROUND AND PURPOSE: The enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) hydrolyze endogenous cannabinoids (eCBs), N-arachidonoyl ethanolamine (AEA) and 2-arachidonoyl glycerol (2-AG), respectively.	aea	176-179	monoglyceride lipase	Mus musculus	74-97
27109320-1	2016	BACKGROUND AND PURPOSE: The enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) hydrolyze endogenous cannabinoids (eCBs), N-arachidonoyl ethanolamine (AEA) and 2-arachidonoyl glycerol (2-AG), respectively.	aea	176-179	monoglyceride lipase	Mus musculus	99-103
27001846-2	2016	We tested whether genetic alterations in endocannabinoid signaling related to a common polymorphism in fatty acid amide hydrolase (FAAH), which alters endocannabinoid anandamide (AEA) levels, would impact the development of frontolimbic circuitry implicated in anxiety disorders.	aea	179-182	fatty acid amide hydrolase	Mus musculus	114-129
27001846-2	2016	We tested whether genetic alterations in endocannabinoid signaling related to a common polymorphism in fatty acid amide hydrolase (FAAH), which alters endocannabinoid anandamide (AEA) levels, would impact the development of frontolimbic circuitry implicated in anxiety disorders.	aea	179-182	fatty acid amide hydrolase	Mus musculus	131-135
27001846-4	2016	Using a knock-in mouse model of the FAAH polymorphism that controls for genetic and environmental backgrounds, we confirm phenotypic differences in frontoamygdala circuitry and anxiety-related behavior by postnatal day 45 (P45), when AEA levels begin to decrease, and also, at P75 but not before.	aea	234-237	fatty acid amide hydrolase	Mus musculus	36-40
27307500-1	2016	Whereas the inhibition of fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL), the respective major hydrolytic enzymes of N-arachidonoyl ethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), elicits no or partial substitution for Delta(9)-tetrahydrocannabinol (THC) in drug-discrimination procedures, combined inhibition of both enzymes fully substitutes for THC, as well as produces a constellation of cannabimimetic effects.	aea	138-165	fatty acid amide hydrolase	Mus musculus	37-52
27307500-1	2016	Whereas the inhibition of fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL), the respective major hydrolytic enzymes of N-arachidonoyl ethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), elicits no or partial substitution for Delta(9)-tetrahydrocannabinol (THC) in drug-discrimination procedures, combined inhibition of both enzymes fully substitutes for THC, as well as produces a constellation of cannabimimetic effects.	aea	138-165	fatty acid amide hydrolase	Mus musculus	54-58
27307500-1	2016	Whereas the inhibition of fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL), the respective major hydrolytic enzymes of N-arachidonoyl ethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), elicits no or partial substitution for Delta(9)-tetrahydrocannabinol (THC) in drug-discrimination procedures, combined inhibition of both enzymes fully substitutes for THC, as well as produces a constellation of cannabimimetic effects.	aea	138-165	monoglyceride lipase	Mus musculus	63-86
27307500-1	2016	Whereas the inhibition of fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL), the respective major hydrolytic enzymes of N-arachidonoyl ethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), elicits no or partial substitution for Delta(9)-tetrahydrocannabinol (THC) in drug-discrimination procedures, combined inhibition of both enzymes fully substitutes for THC, as well as produces a constellation of cannabimimetic effects.	aea	138-165	monoglyceride lipase	Mus musculus	88-92
27307500-1	2016	Whereas the inhibition of fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL), the respective major hydrolytic enzymes of N-arachidonoyl ethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), elicits no or partial substitution for Delta(9)-tetrahydrocannabinol (THC) in drug-discrimination procedures, combined inhibition of both enzymes fully substitutes for THC, as well as produces a constellation of cannabimimetic effects.	aea	167-171	fatty acid amide hydrolase	Mus musculus	37-52
27307500-1	2016	Whereas the inhibition of fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL), the respective major hydrolytic enzymes of N-arachidonoyl ethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), elicits no or partial substitution for Delta(9)-tetrahydrocannabinol (THC) in drug-discrimination procedures, combined inhibition of both enzymes fully substitutes for THC, as well as produces a constellation of cannabimimetic effects.	aea	167-171	fatty acid amide hydrolase	Mus musculus	54-58
27307500-1	2016	Whereas the inhibition of fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL), the respective major hydrolytic enzymes of N-arachidonoyl ethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), elicits no or partial substitution for Delta(9)-tetrahydrocannabinol (THC) in drug-discrimination procedures, combined inhibition of both enzymes fully substitutes for THC, as well as produces a constellation of cannabimimetic effects.	aea	167-171	monoglyceride lipase	Mus musculus	63-86
27307500-1	2016	Whereas the inhibition of fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL), the respective major hydrolytic enzymes of N-arachidonoyl ethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), elicits no or partial substitution for Delta(9)-tetrahydrocannabinol (THC) in drug-discrimination procedures, combined inhibition of both enzymes fully substitutes for THC, as well as produces a constellation of cannabimimetic effects.	aea	167-171	monoglyceride lipase	Mus musculus	88-92
27000802-5	2016	FAAH hydrolyzes and, as a consequence, inactivates anandamide (AEA), a prominent endocannabinoid.	aea	63-66	fatty acid amide hydrolase	Homo sapiens	0-4
27000802-6	2016	Inhibition of FAAH would lead to increases in the amount of AEA oxidized by cytochrome P450s (P450s).	aea	60-63	fatty acid amide hydrolase	Homo sapiens	14-18
27000802-7	2016	CYP2J2, the major P450 epoxygenase expressed in the heart, is also expressed in the intestine and has previously been reported to oxidize AEA.	aea	138-141	cytochrome P450 family 2 subfamily J member 2	Homo sapiens	0-6
27000802-8	2016	We have investigated the possibility that it may play a role in AEA metabolism in the gut and have demonstrated that purified human CYP2J2 metabolizes AEA to form the 20-hydroxyeicosatetraenoic acid ethanolamide (HETE-EA) and several epoxygenated products, including the 5,6-, 8,9-, 11,12-, and 14,15-epoxyeicosatrienoic acid ethanolamides (EET-EAs), in the reconstituted system.	aea	64-67	cytochrome P450 family 2 subfamily J member 2	Homo sapiens	132-138
27000802-8	2016	We have investigated the possibility that it may play a role in AEA metabolism in the gut and have demonstrated that purified human CYP2J2 metabolizes AEA to form the 20-hydroxyeicosatetraenoic acid ethanolamide (HETE-EA) and several epoxygenated products, including the 5,6-, 8,9-, 11,12-, and 14,15-epoxyeicosatrienoic acid ethanolamides (EET-EAs), in the reconstituted system.	aea	151-154	cytochrome P450 family 2 subfamily J member 2	Homo sapiens	132-138
27000802-10	2016	Human intestinal microsomes, which express CYP2J2, metabolize AEA to give the 5,6-, 8,9-, and 11,12-EET-EAs, as well as 20-HETE-EA.	aea	62-65	cytochrome P450 family 2 subfamily J member 2	Homo sapiens	43-49
27000802-11	2016	Studies using specific P450 inhibitors suggest that although CYP2J2 metabolizes AEA, it is not the primary P450 responsible for AEA metabolism in human intestines.	aea	80-83	cytochrome P450 family 2 subfamily J member 2	Homo sapiens	61-67
26821211-3	2016	We have recently found that the stress-related neuropeptide corticotropin-releasing hormone (CRH), acting through the CRH type 1 receptor (CRHR1), can reduce AEA content by increasing its hydrolysis by the enzyme fatty acid amide hydrolase (FAAH) as well as increase 2-AG contents.	aea	158-161	corticotropin releasing hormone	Rattus norvegicus	118-121
26821211-3	2016	We have recently found that the stress-related neuropeptide corticotropin-releasing hormone (CRH), acting through the CRH type 1 receptor (CRHR1), can reduce AEA content by increasing its hydrolysis by the enzyme fatty acid amide hydrolase (FAAH) as well as increase 2-AG contents.	aea	158-161	corticotropin releasing hormone receptor 1	Rattus norvegicus	139-144
26821211-3	2016	We have recently found that the stress-related neuropeptide corticotropin-releasing hormone (CRH), acting through the CRH type 1 receptor (CRHR1), can reduce AEA content by increasing its hydrolysis by the enzyme fatty acid amide hydrolase (FAAH) as well as increase 2-AG contents.	aea	158-161	fatty-acid amide hydrolase-like	Rattus norvegicus	241-245
26821211-10	2016	Consistent with these data indicating sustained increases in CRH signaling can mediate the effects of chronic elevations in corticosteroids, CRH overexpressing mice also exhibited increased FAAH-mediated AEA hydrolysis in the amygdala and prefrontal cortex compared to wild type.	aea	204-207	corticotropin releasing hormone	Mus musculus	141-144
26821211-10	2016	Consistent with these data indicating sustained increases in CRH signaling can mediate the effects of chronic elevations in corticosteroids, CRH overexpressing mice also exhibited increased FAAH-mediated AEA hydrolysis in the amygdala and prefrontal cortex compared to wild type.	aea	204-207	fatty acid amide hydrolase	Mus musculus	190-194
26507196-4	2016	The goal of the present study was to test whether the growth hormone secretagogue receptor (GHS-R1A) antagonist JMV2959 was able to influence morphine-induced effects on anandamide (N-arachidonoylethanolamine, AEA) and 2-arachidonoylglycerol (2-AG) in the nucleus accumbens shell (NACSh).	aea	182-208	growth hormone secretagogue receptor	Rattus norvegicus	54-90
26189725-2	2016	3T3-L1 preadipocytes have the ability to synthesize and degrade endocannabinoid anandamide (AEA) and their differentiation into adipocytes increases the expression of cannabinoid (CB1) and PPAR-gamma receptors.	aea	92-95	cannabinoid receptor 1 (brain)	Mus musculus	180-183
27141613-12	2016	After EA intervention for 7 days, the expression levels of these four proteins in the EA group, and those of MOR, p-ERK 2 and p-CREB in the AEA group were significantly up-regulated (P &lt; 0.001, P &lt; 0.01, P &lt; 0.05).	aea	140-143	mitogen activated protein kinase 1	Rattus norvegicus	116-121
27141613-12	2016	After EA intervention for 7 days, the expression levels of these four proteins in the EA group, and those of MOR, p-ERK 2 and p-CREB in the AEA group were significantly up-regulated (P &lt; 0.001, P &lt; 0.01, P &lt; 0.05).	aea	140-143	cAMP responsive element binding protein 1	Rattus norvegicus	128-132
26486522-13	2016	AEA improves burn-induced delay in gastric emptying, possibly mediated via the sympathetic-COX-2 pathway.	aea	0-3	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	91-96
26052038-4	2015	Here we describe the development of the novel synthetic CB1 PAM, 6-methyl-3-(2-nitro-1-(thiophen-2-yl)ethyl)-2-phenyl-1H-indole (ZCZ011), which augments the in vitro and in vivo pharmacological actions of the CB1 orthosteric agonists CP55,940 and N-arachidonoylethanolamine (AEA).	aea	247-273	cannabinoid receptor 1 (brain)	Mus musculus	56-59
26052038-4	2015	Here we describe the development of the novel synthetic CB1 PAM, 6-methyl-3-(2-nitro-1-(thiophen-2-yl)ethyl)-2-phenyl-1H-indole (ZCZ011), which augments the in vitro and in vivo pharmacological actions of the CB1 orthosteric agonists CP55,940 and N-arachidonoylethanolamine (AEA).	aea	275-278	cannabinoid receptor 1 (brain)	Mus musculus	56-59
26335727-5	2015	On the other hand, AEA-oxidative metabolism by COX-2 is not merely a mean to inactivate its action, but it yields the formation of a new class of mediators, named prostaglandin-ethanolamides, or prostamides.	aea	19-22	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	47-52
26567045-9	2015	RESULTS: IL-6, IL-8 and MMP-3 (determined only in synovial fibroblasts (SFs)) were downregulated in primary synoviocytes and SFs of RA and OA after AEA, PEA and OEA treatment.	aea	148-151	interleukin 6	Mus musculus	9-13
26567045-9	2015	RESULTS: IL-6, IL-8 and MMP-3 (determined only in synovial fibroblasts (SFs)) were downregulated in primary synoviocytes and SFs of RA and OA after AEA, PEA and OEA treatment.	aea	148-151	chemokine (C-X-C motif) ligand 15	Mus musculus	15-19
26567045-9	2015	RESULTS: IL-6, IL-8 and MMP-3 (determined only in synovial fibroblasts (SFs)) were downregulated in primary synoviocytes and SFs of RA and OA after AEA, PEA and OEA treatment.	aea	148-151	matrix metallopeptidase 3	Mus musculus	24-29
26567045-11	2015	FAAH inhibition increased the efficacy of AEA in primary synoviocytes but not in SFs.	aea	42-45	fatty acid amide hydrolase	Mus musculus	0-4
26335727-6	2015	In this study we found that AEA-induced apoptosis in decidual cells involves COX-2 metabolic pathway.	aea	28-31	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	77-82
26335727-7	2015	AEA induced COX-2 expression through p38 MAPK, resulting in the formation of prostamide E2 (PME2).	aea	0-3	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	12-17
25998048-1	2015	Inhibition of fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL), the primary hydrolytic enzymes for the respective endocannabinoids N-arachidonoylethanolamine (AEA) and 2-arachidonylglycerol (2-AG), produces antinociception but with minimal cannabimimetic side effects.	aea	150-176	monoglyceride lipase	Mus musculus	51-74
25998048-1	2015	Inhibition of fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL), the primary hydrolytic enzymes for the respective endocannabinoids N-arachidonoylethanolamine (AEA) and 2-arachidonylglycerol (2-AG), produces antinociception but with minimal cannabimimetic side effects.	aea	150-176	monoglyceride lipase	Mus musculus	76-80
25998048-1	2015	Inhibition of fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL), the primary hydrolytic enzymes for the respective endocannabinoids N-arachidonoylethanolamine (AEA) and 2-arachidonylglycerol (2-AG), produces antinociception but with minimal cannabimimetic side effects.	aea	150-176	fatty acid amide hydrolase	Mus musculus	14-40
25998048-1	2015	Inhibition of fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL), the primary hydrolytic enzymes for the respective endocannabinoids N-arachidonoylethanolamine (AEA) and 2-arachidonylglycerol (2-AG), produces antinociception but with minimal cannabimimetic side effects.	aea	178-181	fatty acid amide hydrolase	Mus musculus	14-40
25998048-1	2015	Inhibition of fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL), the primary hydrolytic enzymes for the respective endocannabinoids N-arachidonoylethanolamine (AEA) and 2-arachidonylglycerol (2-AG), produces antinociception but with minimal cannabimimetic side effects.	aea	150-176	fatty acid amide hydrolase	Mus musculus	42-46
25998048-1	2015	Inhibition of fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL), the primary hydrolytic enzymes for the respective endocannabinoids N-arachidonoylethanolamine (AEA) and 2-arachidonylglycerol (2-AG), produces antinociception but with minimal cannabimimetic side effects.	aea	178-181	fatty acid amide hydrolase	Mus musculus	42-46
25998048-1	2015	Inhibition of fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL), the primary hydrolytic enzymes for the respective endocannabinoids N-arachidonoylethanolamine (AEA) and 2-arachidonylglycerol (2-AG), produces antinociception but with minimal cannabimimetic side effects.	aea	178-181	monoglyceride lipase	Mus musculus	51-74
25998048-1	2015	Inhibition of fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL), the primary hydrolytic enzymes for the respective endocannabinoids N-arachidonoylethanolamine (AEA) and 2-arachidonylglycerol (2-AG), produces antinociception but with minimal cannabimimetic side effects.	aea	178-181	monoglyceride lipase	Mus musculus	76-80
25995819-6	2015	The difference between AEA and NADA in the regulation of adipogenesis is associated with their effects on PPARgamma transactivation.	aea	23-26	peroxisome proliferator activated receptor gamma	Homo sapiens	106-115
25975960-5	2015	Levels of two enzymes participating in the biosynthesis and degradation of AEA, N-acyl-phosphatidylethanolamine-hydrolyzing phospholipase D (NPLD) and fatty acid amide hydrolase (FAAH), together with the most abundant ceramide synthases (CerS1, CerS2, CerS5 and CerS6) in the colon were also determined.	aea	75-78	N-acyl phosphatidylethanolamine phospholipase D	Homo sapiens	80-139
25975960-5	2015	Levels of two enzymes participating in the biosynthesis and degradation of AEA, N-acyl-phosphatidylethanolamine-hydrolyzing phospholipase D (NPLD) and fatty acid amide hydrolase (FAAH), together with the most abundant ceramide synthases (CerS1, CerS2, CerS5 and CerS6) in the colon were also determined.	aea	75-78	fatty acid amide hydrolase	Homo sapiens	179-183
25975960-5	2015	Levels of two enzymes participating in the biosynthesis and degradation of AEA, N-acyl-phosphatidylethanolamine-hydrolyzing phospholipase D (NPLD) and fatty acid amide hydrolase (FAAH), together with the most abundant ceramide synthases (CerS1, CerS2, CerS5 and CerS6) in the colon were also determined.	aea	75-78	ceramide synthase 1	Homo sapiens	238-243
25975960-5	2015	Levels of two enzymes participating in the biosynthesis and degradation of AEA, N-acyl-phosphatidylethanolamine-hydrolyzing phospholipase D (NPLD) and fatty acid amide hydrolase (FAAH), together with the most abundant ceramide synthases (CerS1, CerS2, CerS5 and CerS6) in the colon were also determined.	aea	75-78	ceramide synthase 2	Homo sapiens	245-250
25975960-5	2015	Levels of two enzymes participating in the biosynthesis and degradation of AEA, N-acyl-phosphatidylethanolamine-hydrolyzing phospholipase D (NPLD) and fatty acid amide hydrolase (FAAH), together with the most abundant ceramide synthases (CerS1, CerS2, CerS5 and CerS6) in the colon were also determined.	aea	75-78	ceramide synthase 5	Homo sapiens	252-257
25975960-5	2015	Levels of two enzymes participating in the biosynthesis and degradation of AEA, N-acyl-phosphatidylethanolamine-hydrolyzing phospholipase D (NPLD) and fatty acid amide hydrolase (FAAH), together with the most abundant ceramide synthases (CerS1, CerS2, CerS5 and CerS6) in the colon were also determined.	aea	75-78	ceramide synthase 6	Homo sapiens	262-267
25943894-5	2015	In activated cells, anandamide (AEA), acting as an immune-modulator, suppresses Tat B effect through MKP-1 but Tat C action via MEK-1.	aea	32-35	tyrosine aminotransferase	Homo sapiens	80-83
25943894-5	2015	In activated cells, anandamide (AEA), acting as an immune-modulator, suppresses Tat B effect through MKP-1 but Tat C action via MEK-1.	aea	32-35	dual specificity phosphatase 1	Homo sapiens	101-106
25943894-5	2015	In activated cells, anandamide (AEA), acting as an immune-modulator, suppresses Tat B effect through MKP-1 but Tat C action via MEK-1.	aea	32-35	tyrosine aminotransferase	Homo sapiens	111-114
25943894-5	2015	In activated cells, anandamide (AEA), acting as an immune-modulator, suppresses Tat B effect through MKP-1 but Tat C action via MEK-1.	aea	32-35	mitogen-activated protein kinase kinase 1	Homo sapiens	128-133
25943894-6	2015	AEA lowers nuclear NF-kappaB and TAB2 for both variants while elevating IRAK1BP1 in activated Muller glia.	aea	0-3	interleukin 1 receptor associated kinase 1 binding protein 1	Homo sapiens	72-80
25943894-8	2015	Tat-induced increase in leukocyte adhesion to Muller cells can be mitigated by AEA, involving both CB receptors.	aea	79-82	tyrosine aminotransferase	Homo sapiens	0-3
25995819-7	2015	AEA can directly activate PPARgamma.	aea	0-3	peroxisome proliferator activated receptor gamma	Homo sapiens	26-35
25995819-8	2015	The effect of AEA on PPARgamma in hBM-MSCs may prevail over that on the CB1 receptor mediated signal transduction, giving rise to the AEA-induced promotion of adipogenesis.	aea	14-17	peroxisome proliferator activated receptor gamma	Homo sapiens	21-30
25995819-8	2015	The effect of AEA on PPARgamma in hBM-MSCs may prevail over that on the CB1 receptor mediated signal transduction, giving rise to the AEA-induced promotion of adipogenesis.	aea	134-137	peroxisome proliferator activated receptor gamma	Homo sapiens	21-30
25995819-8	2015	The effect of AEA on PPARgamma in hBM-MSCs may prevail over that on the CB1 receptor mediated signal transduction, giving rise to the AEA-induced promotion of adipogenesis.	aea	134-137	cannabinoid receptor 1	Homo sapiens	72-75
25374388-2	2015	Fatty acid amide hydrolase (FAAH) is primarily responsible for degradation of AEA, and deletion of FAAH increases AEA content in various tissues.	aea	78-81	fatty acid amide hydrolase	Mus musculus	11-26
25374388-2	2015	Fatty acid amide hydrolase (FAAH) is primarily responsible for degradation of AEA, and deletion of FAAH increases AEA content in various tissues.	aea	78-81	fatty acid amide hydrolase	Mus musculus	28-32
25374388-2	2015	Fatty acid amide hydrolase (FAAH) is primarily responsible for degradation of AEA, and deletion of FAAH increases AEA content in various tissues.	aea	114-117	fatty acid amide hydrolase	Mus musculus	11-26
25374388-2	2015	Fatty acid amide hydrolase (FAAH) is primarily responsible for degradation of AEA, and deletion of FAAH increases AEA content in various tissues.	aea	114-117	fatty acid amide hydrolase	Mus musculus	28-32
25374388-2	2015	Fatty acid amide hydrolase (FAAH) is primarily responsible for degradation of AEA, and deletion of FAAH increases AEA content in various tissues.	aea	114-117	fatty acid amide hydrolase	Mus musculus	99-103