PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 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 108-134 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 32041998-7 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 23347118-11 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 157-160 fatty acid amide hydrolase Homo sapiens 92-96 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 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 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