PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 30114402-4 2018 A major endocannabinoid, anandamide (N-arachidonoylethanolamine, AEA), is metabolized by fatty acid amide hydrolase (FAAH). Endocannabinoids 8-23 fatty acid amide hydrolase Homo sapiens 117-121 29729263-7 2018 To date, the most investigated compounds are inhibitors of fatty acid amide hydrolase (FAAH), an enzyme that degrades the endocannabinoid anandamide. Endocannabinoids 122-137 fatty acid amide hydrolase Homo sapiens 59-85 29729263-7 2018 To date, the most investigated compounds are inhibitors of fatty acid amide hydrolase (FAAH), an enzyme that degrades the endocannabinoid anandamide. Endocannabinoids 122-137 fatty acid amide hydrolase Homo sapiens 87-91 29695817-2 2018 Pharmacological inhibition of endocannabinoid-degrading enzymes, such as fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL), elicit promising anxiolytic effects in rodent models with limited adverse behavioral effects, however, the efficacy of dual FAAH/MAGL inhibition has not been investigated. Endocannabinoids 30-45 fatty acid amide hydrolase Homo sapiens 73-99 29695817-2 2018 Pharmacological inhibition of endocannabinoid-degrading enzymes, such as fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL), elicit promising anxiolytic effects in rodent models with limited adverse behavioral effects, however, the efficacy of dual FAAH/MAGL inhibition has not been investigated. Endocannabinoids 30-45 fatty acid amide hydrolase Homo sapiens 101-105 29695817-2 2018 Pharmacological inhibition of endocannabinoid-degrading enzymes, such as fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL), elicit promising anxiolytic effects in rodent models with limited adverse behavioral effects, however, the efficacy of dual FAAH/MAGL inhibition has not been investigated. Endocannabinoids 30-45 fatty acid amide hydrolase Homo sapiens 267-271 27309570-2 2016 In particular, indirectly enhancing endocannabinoid signaling to therapeutic levels through FAAH inhibition might be beneficial for neurodegenerative disorders such as Alzheimer"s disease, effectively preventing or slowing the progression of the disease. Endocannabinoids 36-51 fatty acid amide hydrolase Homo sapiens 92-96 28150397-2 2018 One of the two main endocannabinoid neurotransmitters, anandamide, is metabolized by fatty acid amide hydrolase, an enzyme with a functional genetic polymorphism (FAAH Pro129Thr, rs324420). Endocannabinoids 20-35 fatty acid amide hydrolase Homo sapiens 163-167 27806235-1 2016 BACKGROUND: A decrease in fatty acid amide hydrolase (FAAH) activity increases the levels of endogenous analogues of cannabinoids, or endocannabinoids. Endocannabinoids 134-150 fatty acid amide hydrolase Homo sapiens 54-58 27582708-7 2016 Therefore, in the present review, we summarize the role of dual-acting molecules (FAAH/TRPV1 and FAAH/COX-2 inhibitors) that interact with endocannabinoid and endovanillinoid systems and act as analgesics by elevating the endogenously produced endocannabinoids and dampening the production of pro-inflammatory prostaglandins. Endocannabinoids 139-154 fatty acid amide hydrolase Homo sapiens 82-86 27582708-7 2016 Therefore, in the present review, we summarize the role of dual-acting molecules (FAAH/TRPV1 and FAAH/COX-2 inhibitors) that interact with endocannabinoid and endovanillinoid systems and act as analgesics by elevating the endogenously produced endocannabinoids and dampening the production of pro-inflammatory prostaglandins. Endocannabinoids 139-154 fatty acid amide hydrolase Homo sapiens 97-101 27989417-1 2017 The serine hydrolase fatty acid amide hydrolase (FAAH) catalyzes the degradation of the endocannabinoid anandamide, which possesses analgesic and anti-inflammatory effects. Endocannabinoids 88-103 fatty acid amide hydrolase Homo sapiens 21-47 27989417-1 2017 The serine hydrolase fatty acid amide hydrolase (FAAH) catalyzes the degradation of the endocannabinoid anandamide, which possesses analgesic and anti-inflammatory effects. Endocannabinoids 88-103 fatty acid amide hydrolase Homo sapiens 49-53 27309570-3 2016 Hence, in the search for a more effective treatment for Alzheimer"s disease, in this paper, the multitarget-directed ligand paradigm was applied to the design of carbamates able to simultaneously target the recently proposed endocannabinoid system and the classic cholinesterase system, and achieve effective dual FAAH/cholinesterase inhibitors. Endocannabinoids 225-240 fatty acid amide hydrolase Homo sapiens 314-318 27000802-5 2016 FAAH hydrolyzes and, as a consequence, inactivates anandamide (AEA), a prominent endocannabinoid. Endocannabinoids 81-96 fatty acid amide hydrolase Homo sapiens 0-4 24705380-1 2014 The endocannabinoid anandamide (AEA) is an antinociceptive lipid that is inactivated through cellular uptake and subsequent catabolism by fatty acid amide hydrolase (FAAH). Endocannabinoids 4-19 fatty acid amide hydrolase Homo sapiens 166-170 26505525-1 2016 Fatty acid amide hydrolase (FAAH) is one of the principle enzymes for metabolizing endogenous cannabinoid neurotransmitters such as anandamide, and thus regulates endocannabinoid (eCB) signaling. Endocannabinoids 163-178 fatty acid amide hydrolase Homo sapiens 28-32 26505525-1 2016 Fatty acid amide hydrolase (FAAH) is one of the principle enzymes for metabolizing endogenous cannabinoid neurotransmitters such as anandamide, and thus regulates endocannabinoid (eCB) signaling. Endocannabinoids 180-183 fatty acid amide hydrolase Homo sapiens 28-32 26561012-4 2015 We investigated a multiethnic Brazilian population to study the relationships among the polymorphism 385C>A in an endocannabinoid degrading enzyme gene (FAAH), endocannabinoid levels and markers of cardiometabolic risk. Endocannabinoids 117-132 fatty acid amide hydrolase Homo sapiens 156-160 26561012-10 2015 Our findings provide evidence for an endocannabinoid-related phenotype that may be identified by the combination of circulating anandamide levels with genotyping of the FAAH 385C>A; this phenotype is not exclusive to mono-ethnoracial populations nor to individuals with severe obesity. Endocannabinoids 37-52 fatty acid amide hydrolase Homo sapiens 169-173 25731744-2 2015 We developed a knock-in mouse that biologically recapitulates a common human mutation in the gene for fatty acid amide hydrolase (FAAH) (C385A; rs324420), the primary catabolic enzyme for the endocannabinoid anandamide. Endocannabinoids 192-207 fatty acid amide hydrolase Homo sapiens 130-134 26413912-1 2015 INTRODUCTION: Fatty acid amide hydrolase (FAAH) is a key enzyme responsible for the degradation of the endocannabinoid anandamide. Endocannabinoids 103-118 fatty acid amide hydrolase Homo sapiens 14-40 26413912-1 2015 INTRODUCTION: Fatty acid amide hydrolase (FAAH) is a key enzyme responsible for the degradation of the endocannabinoid anandamide. Endocannabinoids 103-118 fatty acid amide hydrolase Homo sapiens 42-46 25283614-1 2014 Besides the suggested role of a putative endocannabinoid membrane transporter mediating the cellular uptake of the endocannabinoid anandamide (AEA), this process is intrinsically coupled to AEA degradation by the fatty acid amide hydrolase (FAAH). Endocannabinoids 41-56 fatty acid amide hydrolase Homo sapiens 241-245 26808012-1 2016 Fatty acid amide hydrolase (FAAH) metabolizes the endocannabinoid anandamide, which has an important role in nociception. Endocannabinoids 50-65 fatty acid amide hydrolase Homo sapiens 28-32 26082009-1 2015 Positron emission tomography with [(11)C]CURB was recently developed to quantify fatty acid amide hydrolase (FAAH), the enzyme responsible for hydrolyzing the endocannabinoid anandamide. Endocannabinoids 159-174 fatty acid amide hydrolase Homo sapiens 81-107 26082009-1 2015 Positron emission tomography with [(11)C]CURB was recently developed to quantify fatty acid amide hydrolase (FAAH), the enzyme responsible for hydrolyzing the endocannabinoid anandamide. Endocannabinoids 159-174 fatty acid amide hydrolase Homo sapiens 109-113 26263913-2 2015 The present study focused on inhibitors of the enzyme fatty acid amide hydrolase (FAAH), which catalyzes the degradation of endocannabinoids (anandamide, 2-arachidonoylglycerol) and endocannabinoid-like substances (N-oleoylethanolamine, N-palmitoylethanolamine). Endocannabinoids 124-140 fatty acid amide hydrolase Homo sapiens 82-86 26263913-2 2015 The present study focused on inhibitors of the enzyme fatty acid amide hydrolase (FAAH), which catalyzes the degradation of endocannabinoids (anandamide, 2-arachidonoylglycerol) and endocannabinoid-like substances (N-oleoylethanolamine, N-palmitoylethanolamine). Endocannabinoids 124-139 fatty acid amide hydrolase Homo sapiens 82-86 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. Endocannabinoids 88-103 fatty acid amide hydrolase Homo sapiens 55-59 26408159-1 2015 The endocannabinoids anandamide and 2-arachidonoylglycerol are metabolised by both hydrolytic enzymes (primarily fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MGL)) and oxygenating enzymes (e.g. cyclooxygenase-2, COX-2). Endocannabinoids 4-20 fatty acid amide hydrolase Homo sapiens 141-145 22688188-2 2013 The endocannabinoid anandamide is degraded by the catabolic enzyme fatty acid amide hydrolase (FAAH). Endocannabinoids 4-19 fatty acid amide hydrolase Homo sapiens 95-99 24445122-0 2013 Effects of C358A polymorphism of the endocannabinoid degrading enzyme fatty acid amide hydrolase (FAAH) on weight loss, adipocytokines levels, and insulin resistance after a high polyunsaturated fat diet in obese patients. Endocannabinoids 37-52 fatty acid amide hydrolase Homo sapiens 98-102 24223930-2 2013 Anandamide (AEA) is an endocannabinoid that is inactivated by cellular uptake followed by intracellular hydrolysis by fatty acid amide hydrolase (FAAH). Endocannabinoids 23-38 fatty acid amide hydrolase Homo sapiens 146-150 23333123-0 2013 Genetic variation in the endocannabinoid degrading enzyme fatty acid amide hydrolase (FAAH) and their influence on weight loss and insulin resistance under a high monounsaturated fat hypocaloric diet. Endocannabinoids 25-40 fatty acid amide hydrolase Homo sapiens 86-90 23344792-7 2013 The data suggest that interactions of FAAH inhibitors with albumin may provide added advantages for their ability to modulate endocannabinoid levels for a range of applications including analgesia, antiemesis, and neuroprotection. Endocannabinoids 126-141 fatty acid amide hydrolase Homo sapiens 38-42 22146559-1 2012 Fatty acid amide hydrolase (FAAH) is the main enzyme responsible for the hydrolysis of the endocannabinoid anandamide (arachidonoyl ethanolamide, AEA) to arachidonic acid (AA) and ethanolamine (EA). Endocannabinoids 91-106 fatty acid amide hydrolase Homo sapiens 28-32 22776995-0 2012 A polymorphism in the gene of the endocannabinoid-degrading enzyme FAAH (FAAH C385A) is associated with emotional-motivational reactivity. Endocannabinoids 34-49 fatty acid amide hydrolase Homo sapiens 67-71 22776995-0 2012 A polymorphism in the gene of the endocannabinoid-degrading enzyme FAAH (FAAH C385A) is associated with emotional-motivational reactivity. Endocannabinoids 34-49 fatty acid amide hydrolase Homo sapiens 73-77 22776995-2 2012 Investigating emotional-motivational dysfunctions as underlying mechanisms, a study in humans revealed that in the C385A polymorphism of the fatty acid amide hydrolase (FAAH), the degrading enzyme of the eCB anandamide (AEA), A carriers, who are characterized by increased signaling of AEA as compared to C/C carriers, exhibited reduced brain reactivity towards unpleasant faces and enhanced reactivity towards reward. Endocannabinoids 204-207 fatty acid amide hydrolase Homo sapiens 141-167 22776995-2 2012 Investigating emotional-motivational dysfunctions as underlying mechanisms, a study in humans revealed that in the C385A polymorphism of the fatty acid amide hydrolase (FAAH), the degrading enzyme of the eCB anandamide (AEA), A carriers, who are characterized by increased signaling of AEA as compared to C/C carriers, exhibited reduced brain reactivity towards unpleasant faces and enhanced reactivity towards reward. Endocannabinoids 204-207 fatty acid amide hydrolase Homo sapiens 169-173 22609216-0 2012 Relationship among metabolic syndrome, C358A polymorphism of the endocannabinoid degrading enzyme fatty acid amide hydrolase (FAAH) and insulin resistance. Endocannabinoids 65-80 fatty acid amide hydrolase Homo sapiens 98-124 22609216-0 2012 Relationship among metabolic syndrome, C358A polymorphism of the endocannabinoid degrading enzyme fatty acid amide hydrolase (FAAH) and insulin resistance. Endocannabinoids 65-80 fatty acid amide hydrolase Homo sapiens 126-130 23409303-0 2004 6-Hydroxy-[1,1"-biphenyl]-3-yl-cyclohexyl-[(11)C-carbonyl]carbamate Fatty acid amide hydrolase (FAAH) is an integral membrane-bound serine hydrolase and a part of the endocannabinoid system (ECS), which comprises the cannabinoid receptors (CB1 and CB2), endogenous ligands termed endocannabinoids (anandamide and oleamide), transporters, and enzymes (1, 2). Endocannabinoids 280-296 fatty acid amide hydrolase Homo sapiens 96-100 22624680-2 2012 Anandamide and N-arachidonoyl dopamine (NA-DA), endocannabinoids that activate TRPV1 or are metabolized by FAAH, also inhibit T-type calcium channels (I(Ca) ). Endocannabinoids 48-64 fatty acid amide hydrolase Homo sapiens 107-111 22701012-10 2012 Cannabinoid receptors and endocannabinoid modulating enzymes were localized in fallopian tube epithelium by immunohistochemistry and showed reduced CB1 and FAAH expression in ectopic pregnancy. Endocannabinoids 26-41 fatty acid amide hydrolase Homo sapiens 156-160 22133920-1 2012 Fatty acid amide hydrolase (FAAH) is an enzyme that metabolizes endocannabinoids and fatty acid amides possibly linked to activation of the opioid system. Endocannabinoids 64-80 fatty acid amide hydrolase Homo sapiens 0-26 22133920-1 2012 Fatty acid amide hydrolase (FAAH) is an enzyme that metabolizes endocannabinoids and fatty acid amides possibly linked to activation of the opioid system. Endocannabinoids 64-80 fatty acid amide hydrolase Homo sapiens 28-32 21442624-1 2012 Fatty acid amide hydrolase (FAAH), the enzyme responsible for the degradation of the main endocannabinoid, anandamide, and related fatty acid amides, has emerged as a regulator of endocannabinoid signaling. Endocannabinoids 90-105 fatty acid amide hydrolase Homo sapiens 28-32 21645511-1 2011 Fatty acid amide hydrolase (FAAH) hydrolyzes several bioactive lipids including the endocannabinoid anandamide. Endocannabinoids 84-99 fatty acid amide hydrolase Homo sapiens 28-32 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. Endocannabinoids 155-170 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. Endocannabinoids 155-170 fatty acid amide hydrolase Homo sapiens 28-32 21930339-2 2012 OBJECTIVE: Investigate the expression of the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH) in human, rat, and mouse bladders and study the effects of inhibition of FAAH during urodynamics in awake rats. Endocannabinoids 45-60 fatty acid amide hydrolase Homo sapiens 78-104 21930339-2 2012 OBJECTIVE: Investigate the expression of the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH) in human, rat, and mouse bladders and study the effects of inhibition of FAAH during urodynamics in awake rats. Endocannabinoids 45-60 fatty acid amide hydrolase Homo sapiens 106-110 21501143-3 2011 FAAH hydrolyses the endogenous endocannabinoid anandamide, as well as other non-cannabinoid ligands such as oleoylethanolamide (OEA) and palmitoylethanolamide (PEA). Endocannabinoids 31-46 fatty acid amide hydrolase Homo sapiens 0-4 21631410-1 2011 Fatty acid amide hydrolase (FAAH) is responsible for hydrolysis of endocannabinoid, anandamide (AEA), and N-acyl ethanolamines such as palmitoylethanolamine (PEA) and N-oleoylethanolamide (OEA). Endocannabinoids 67-82 fatty acid amide hydrolase Homo sapiens 28-32 21666860-1 2011 Fatty acid amide hydrolase (FAAH) is an integral membrane serine hydrolase that degrades the fatty acid amide family of signaling lipids, including the endocannabinoid anandamide. Endocannabinoids 152-167 fatty acid amide hydrolase Homo sapiens 28-32 21505060-1 2011 The endogenous cannabinoid (endocannabinoid) anandamide is principally degraded by the integral membrane enzyme fatty acid amide hydrolase (FAAH). Endocannabinoids 28-43 fatty acid amide hydrolase Homo sapiens 140-144 22295023-2 2011 The biological effects of cannabinoids are limited by the activation of the endocannabinoid degrading enzyme fatty acid amide hydrolase (FAAH). Endocannabinoids 76-91 fatty acid amide hydrolase Homo sapiens 109-135 22295023-2 2011 The biological effects of cannabinoids are limited by the activation of the endocannabinoid degrading enzyme fatty acid amide hydrolase (FAAH). Endocannabinoids 76-91 fatty acid amide hydrolase Homo sapiens 137-141 20808855-2 2010 Here we have investigated the expression of the endocannabinoid metabolising enzyme fatty acid amide hydrolase (FAAH) in a well characterised tissue microarray from patients diagnosed with prostate cancer at transurethral resection for voiding problems. Endocannabinoids 48-63 fatty acid amide hydrolase Homo sapiens 112-116 21519771-0 2010 Relation of C358A polymorphism of the endocannabinoid degrading enzyme fatty acid amide hydrolase (FAAH) with obesity and insulin resistance. Endocannabinoids 38-53 fatty acid amide hydrolase Homo sapiens 71-97 21519771-0 2010 Relation of C358A polymorphism of the endocannabinoid degrading enzyme fatty acid amide hydrolase (FAAH) with obesity and insulin resistance. Endocannabinoids 38-53 fatty acid amide hydrolase Homo sapiens 99-103 20056290-0 2010 C358A missense polymorphism of the endocannabinoid degrading enzyme fatty acid amide hydrolase (FAAH) and insulin resistance in patients with diabetes mellitus type 2. Endocannabinoids 35-50 fatty acid amide hydrolase Homo sapiens 96-100 20653671-3 2010 WHAT THIS PAPER ADDS: The data presented in this manuscript clearly show that the endocannabinoid 2-arrachidonyl glycerol can activate platelet activity, but that the effects are mediated through an aspirin-sensitive pathway that is not affected by cannabinoid receptor antagonists or FAAH inhibition, but is abolished by MAGL inhibition. Endocannabinoids 82-97 fatty acid amide hydrolase Homo sapiens 285-289 20493882-2 2010 URB597 is one of the best characterized covalent inhibitors of the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH). Endocannabinoids 67-82 fatty acid amide hydrolase Homo sapiens 128-132 20189896-0 2010 [C358A polymorphism of the endocannabinoid degrading enzyme fatty acid amide hydrolase (FAAH) and adipocytokine levels in the morbidly obese]. Endocannabinoids 27-42 fatty acid amide hydrolase Homo sapiens 88-92 20065978-0 2010 C358A missense polymorphism of the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH) and visfatin levels in obese females. Endocannabinoids 35-50 fatty acid amide hydrolase Homo sapiens 68-94 20065978-0 2010 C358A missense polymorphism of the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH) and visfatin levels in obese females. Endocannabinoids 35-50 fatty acid amide hydrolase Homo sapiens 96-100 19811221-10 2009 In conclusion, the endocannabinoid 2-AG, as well as other 2-acylglycerols, are substrates of both FAAH and MAGL; the latter was characterized for the first time in platelets. Endocannabinoids 19-34 fatty acid amide hydrolase Homo sapiens 98-102 20044928-1 2010 BACKGROUND: The orexigenic effects of cannabinoids are limited by activation of the endocannabinoid degrading enzyme fatty acid amide hydrolase (FAAH). Endocannabinoids 84-99 fatty acid amide hydrolase Homo sapiens 145-149 19559363-4 2009 In particular, it appears that the endocannabinoid-degrading enzyme FAAH (fatty acid amide hydrolase) has a central role in this array of signals, because it controls several steps of sperm biology, from motility to capacitation and acrosome reaction. Endocannabinoids 35-50 fatty acid amide hydrolase Homo sapiens 68-72 19559363-4 2009 In particular, it appears that the endocannabinoid-degrading enzyme FAAH (fatty acid amide hydrolase) has a central role in this array of signals, because it controls several steps of sperm biology, from motility to capacitation and acrosome reaction. Endocannabinoids 35-50 fatty acid amide hydrolase Homo sapiens 74-100 20544003-1 2009 BACKGROUND: Fatty acid amide hydrolase (FAAH) is an integral membrane enzyme that hydrolyzes the endocannabinoid anandamide and related amidated signaling lipids. Endocannabinoids 97-112 fatty acid amide hydrolase Homo sapiens 12-38 19103437-1 2009 BACKGROUND: Fatty acid amide hydrolase (FAAH) is a key enzyme in regulating endocannabinoid (eCB) signaling. Endocannabinoids 76-91 fatty acid amide hydrolase Homo sapiens 12-38 19103437-1 2009 BACKGROUND: Fatty acid amide hydrolase (FAAH) is a key enzyme in regulating endocannabinoid (eCB) signaling. Endocannabinoids 76-91 fatty acid amide hydrolase Homo sapiens 40-44 19103437-1 2009 BACKGROUND: Fatty acid amide hydrolase (FAAH) is a key enzyme in regulating endocannabinoid (eCB) signaling. Endocannabinoids 93-96 fatty acid amide hydrolase Homo sapiens 12-38 19103437-1 2009 BACKGROUND: Fatty acid amide hydrolase (FAAH) is a key enzyme in regulating endocannabinoid (eCB) signaling. Endocannabinoids 93-96 fatty acid amide hydrolase Homo sapiens 40-44 20544003-1 2009 BACKGROUND: Fatty acid amide hydrolase (FAAH) is an integral membrane enzyme that hydrolyzes the endocannabinoid anandamide and related amidated signaling lipids. Endocannabinoids 97-112 fatty acid amide hydrolase Homo sapiens 40-44 19607961-11 2009 The reason why FAAH inhibition approach produces a smaller set of cannabimimetic effects might depend on the mechanism of EC synthesis and release upon neuronal activation and on the target selectivity of the drug. Endocannabinoids 122-124 fatty acid amide hydrolase Homo sapiens 15-19 19389627-2 2009 The endocannabinoid anandamide is principally degraded by the integral membrane enzyme fatty acid amide hydrolase (FAAH), and there is currently much interest in developing FAAH inhibitors to augment endocannabinoid signaling in vivo. Endocannabinoids 4-19 fatty acid amide hydrolase Homo sapiens 115-119 19389627-2 2009 The endocannabinoid anandamide is principally degraded by the integral membrane enzyme fatty acid amide hydrolase (FAAH), and there is currently much interest in developing FAAH inhibitors to augment endocannabinoid signaling in vivo. Endocannabinoids 200-215 fatty acid amide hydrolase Homo sapiens 115-119 19389627-2 2009 The endocannabinoid anandamide is principally degraded by the integral membrane enzyme fatty acid amide hydrolase (FAAH), and there is currently much interest in developing FAAH inhibitors to augment endocannabinoid signaling in vivo. Endocannabinoids 200-215 fatty acid amide hydrolase Homo sapiens 173-177 19367506-3 2009 Two endocannabinoid deactivating enzymes, fatty acid amide hydrolase (FAAH) and soluble monoacylglycerol lipase (MGL), are increasingly prominent targets for inhibitors that indirectly potentiate endocannabinoid-system signalling. Endocannabinoids 4-19 fatty acid amide hydrolase Homo sapiens 70-74 19675519-8 2009 Endocannabinoids are transported into cells by a specific uptake system and degraded by the enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL). Endocannabinoids 0-16 fatty acid amide hydrolase Homo sapiens 128-132 17177441-1 2006 Fatty acid amide hydrolase (FAAH) is a serine hydrolase that degrades anandamide, an endocannabinoid, and oleamide, a sleep-inducing lipid, and has potential applications as a therapeutic target for neurological disorders. Endocannabinoids 85-100 fatty acid amide hydrolase Homo sapiens 28-32 18805581-0 2008 Nuclear localisation of the endocannabinoid metabolizing enzyme fatty acid amide hydrolase (FAAH) in invasive trophoblasts and an association with recurrent miscarriage. Endocannabinoids 28-43 fatty acid amide hydrolase Homo sapiens 92-96 18805581-2 2008 The endocannabinoid anandamide, is metabolized by the enzyme fatty acid amide hydrolase (FAAH), and insufficient levels of this enzyme have been implicated in spontaneous miscarriage in women and implantation failure in mice. Endocannabinoids 4-19 fatty acid amide hydrolase Homo sapiens 89-93 18497731-1 2008 BACKGROUND: Fatty acid amide hydrolase (FAAH) inhibitors, preventing endocannabinoid (EC) degradation, reduce blood pressure (BP) and heart rate in young male (YM) hypertensive rodents. Endocannabinoids 86-88 fatty acid amide hydrolase Homo sapiens 40-44 17665899-1 2007 Fatty acid amide hydrolase (FAAH) is an intracellular serine hydrolase, which catalyzes the hydrolysis of the endocannabinoid N-arachidonoylethanolamide to arachidonic acid and ethanolamine. Endocannabinoids 110-125 fatty acid amide hydrolase Homo sapiens 28-32 17665899-2 2007 FAAH also hydrolyzes another endocannabinoid, 2-arachidonoylglycerol (2-AG). Endocannabinoids 29-44 fatty acid amide hydrolase Homo sapiens 0-4 18753625-1 2008 The integral membrane enzyme fatty acid amide hydrolase (FAAH) hydrolyzes the endocannabinoid anandamide and related amidated signaling lipids. Endocannabinoids 78-93 fatty acid amide hydrolase Homo sapiens 57-61 18497731-1 2008 BACKGROUND: Fatty acid amide hydrolase (FAAH) inhibitors, preventing endocannabinoid (EC) degradation, reduce blood pressure (BP) and heart rate in young male (YM) hypertensive rodents. Endocannabinoids 69-84 fatty acid amide hydrolase Homo sapiens 12-38 18497731-1 2008 BACKGROUND: Fatty acid amide hydrolase (FAAH) inhibitors, preventing endocannabinoid (EC) degradation, reduce blood pressure (BP) and heart rate in young male (YM) hypertensive rodents. Endocannabinoids 69-84 fatty acid amide hydrolase Homo sapiens 40-44 18497731-1 2008 BACKGROUND: Fatty acid amide hydrolase (FAAH) inhibitors, preventing endocannabinoid (EC) degradation, reduce blood pressure (BP) and heart rate in young male (YM) hypertensive rodents. Endocannabinoids 86-88 fatty acid amide hydrolase Homo sapiens 12-38 18534634-0 2008 Inhibition of fatty acid amide hydrolase and cyclooxygenase-2 increases levels of endocannabinoid related molecules and produces analgesia via peroxisome proliferator-activated receptor-alpha in a model of inflammatory pain. Endocannabinoids 82-97 fatty acid amide hydrolase Homo sapiens 14-40 17962356-2 2008 The endocannabinoid, anandamide, is inactivated by fatty acid amide hydrolase (FAAH). Endocannabinoids 4-19 fatty acid amide hydrolase Homo sapiens 79-83 17935697-2 2007 The most abundant endogenous endocannabinoid, anandamide, has been shown to activate the cannabinoid receptor type 1 (CB1) and type 2 (CB2) as well as the "non-cannabinoid" transient receptor potential channel-vanilloid sub-family member 1 (TRPV1), before being rapidly metabolised by fatty acid amide hydrolase (FAAH). Endocannabinoids 29-44 fatty acid amide hydrolase Homo sapiens 313-317 17083980-1 2007 Fatty acid amide hydrolase (FAAH) is the enzyme responsible for the rapid degradation of fatty acid amides such as the endocannabinoid anandamide. Endocannabinoids 119-134 fatty acid amide hydrolase Homo sapiens 28-32 12781177-1 2003 Three new endocannabinoid analogues in which amide moiety was replaced either by oxomethylene group or ester moiety with simultaneous substitution of both alpha-hydrogens with methyl groups were synthesized and their abilities to interact with CB1-receptor and FAAH were investigated. Endocannabinoids 10-25 fatty acid amide hydrolase Homo sapiens 261-265 15951097-5 2005 In this study the endocannabinoid anandamide, was found to be metabolized by T. pyriformis homogenate by the action of a FAAH-like enzyme, in a time- and concentration-dependent manner. Endocannabinoids 18-33 fatty acid amide hydrolase Homo sapiens 121-125 16298297-1 2005 Fatty acid amide hydrolase (FAAH) regulates a large class of signaling lipids, including the endocannabinoid anandamide. Endocannabinoids 93-108 fatty acid amide hydrolase Homo sapiens 28-32 12799380-2 2003 Physiological concentrations of progesterone stimulate the activity of the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH) in human T lymphocytes, up to a approximately 270% over the untreated controls. Endocannabinoids 75-90 fatty acid amide hydrolase Homo sapiens 136-140 16375688-0 2005 Partial QSAR analysis of some selected natural inhibitors of FAAH suggests a working hypothesis for the development of endocannabinoid-based drugs. Endocannabinoids 119-134 fatty acid amide hydrolase Homo sapiens 61-65 16375688-3 2005 Here we discuss the role of natural endocannabinoid derivatives, like the hydroxy-anandamides (OH-AEAs) generated from AEA via lipoxygenase activity, as powerful inhibitors of FAAH. Endocannabinoids 36-51 fatty acid amide hydrolase Homo sapiens 176-180 16375688-4 2005 We propose that these compounds, by reversibly inhibiting FAAH, may control in vivo the endocannabinoid tone. Endocannabinoids 88-103 fatty acid amide hydrolase Homo sapiens 58-62 15721218-4 2005 The fatty acid amide hydrolase (FAAH) is a primary catabolic enzyme of endocannabinoids. Endocannabinoids 71-87 fatty acid amide hydrolase Homo sapiens 4-30 15721218-4 2005 The fatty acid amide hydrolase (FAAH) is a primary catabolic enzyme of endocannabinoids. Endocannabinoids 71-87 fatty acid amide hydrolase Homo sapiens 32-36 11390466-1 2001 Physiological concentrations of progesterone stimulate the activity of the endocannabinoid-degrading enzyme anandamide hydrolase (fatty acid amide hydrolase, FAAH) in human lymphocytes. Endocannabinoids 75-90 fatty acid amide hydrolase Homo sapiens 158-162 12556536-1 2003 Physiological concentrations of leptin stimulate the activity of the endocannabinoid-degrading enzyme anandamide hydrolase (fatty acid amide hydrolase, FAAH) in human T lymphocytes up to approximately 300% over the untreated controls. Endocannabinoids 69-84 fatty acid amide hydrolase Homo sapiens 152-156 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). Endocannabinoids 136-151 fatty acid amide hydrolase Homo sapiens 59-63 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). Endocannabinoids 153-156 fatty acid amide hydrolase Homo sapiens 59-63 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). Endocannabinoids 206-209 fatty acid amide hydrolase Homo sapiens 59-63 32987725-4 2020 An increasing body of literature describing the interactions between the endocannabinoid system and PPARs has slowly but surely been accumulating over the past decade, and a multitarget approach involving these receptors and endocannabinoid degrading enzyme FAAH has been proposed for the treatment of inflammatory states, cancer, and Alzheimer"s disease. Endocannabinoids 225-240 fatty acid amide hydrolase Homo sapiens 258-262 34496065-2 2022 The fatty acid amide hydrolase (FAAH) C385A polymorphism, which is associated with enhanced endocannabinoid signaling in the brain, has been identified across species as a potential protective factor from anxiety. Endocannabinoids 92-107 fatty acid amide hydrolase Homo sapiens 4-30 34496065-2 2022 The fatty acid amide hydrolase (FAAH) C385A polymorphism, which is associated with enhanced endocannabinoid signaling in the brain, has been identified across species as a potential protective factor from anxiety. Endocannabinoids 92-107 fatty acid amide hydrolase Homo sapiens 32-36 34830856-6 2021 Indeed, a number of studies accordingly showed an inhibitory effect of blockers of the endocannabinoid-degrading enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) on tumour development and spread. Endocannabinoids 87-102 fatty acid amide hydrolase Homo sapiens 121-147 34830856-6 2021 Indeed, a number of studies accordingly showed an inhibitory effect of blockers of the endocannabinoid-degrading enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) on tumour development and spread. Endocannabinoids 87-102 fatty acid amide hydrolase Homo sapiens 149-153 34051704-3 2022 Emerging data indicate that genetic variation in fatty acid amide hydrolase (FAAH C385A; rs324420) is associated with increased peripheral endocannabinoid (eCB) levels and lesser threat-related amygdala reactivity. Endocannabinoids 139-154 fatty acid amide hydrolase Homo sapiens 77-81 32551466-6 2020 Of these, reduction of endocannabinoid degradation via FAAH and/or COX-2 inhibition, accumulation of arachidonic acid to endocannabinoid biosynthesis following COX inhibition, inhibition of cellular uptake of endocannabinoids directly or following inhibition of nitric oxide synthase production, and induction of endocannabinoid release are among the proposed mechanisms. Endocannabinoids 23-38 fatty acid amide hydrolase Homo sapiens 55-59 30226747-4 2019 We report a new multitarget drug, AGN220653, containing a carboxyamide-4-oxazole moiety and endowed with efficacious analgesic and anti-inflammatory activities, which are partly due to its capability of achieving inhibition of FAAH, and subsequently increasing the tissue concentrations of the endocannabinoid anandamide. Endocannabinoids 294-309 fatty acid amide hydrolase Homo sapiens 227-231 31407888-2 2019 Fatty acid amide hydrolase (FAAH) hydrolyzes the endocannabinoid anandamide and other N-acylethanolamines. Endocannabinoids 49-64 fatty acid amide hydrolase Homo sapiens 0-26 31407888-2 2019 Fatty acid amide hydrolase (FAAH) hydrolyzes the endocannabinoid anandamide and other N-acylethanolamines. Endocannabinoids 49-64 fatty acid amide hydrolase Homo sapiens 28-32