INT73342

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Context Info
Confidence 0.97
First Reported 1997
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 19
Total Number 19
Disease Relevance 5.11
Pain Relevance 8.99

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

lipid binding (Faah) Golgi apparatus (Faah) endoplasmic reticulum (Faah)
cytoplasm (Faah)
Anatomy Link Frequency
blood 1
immune system 1
dorsal root ganglion 1
nervous system 1
ventral 1
Faah (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Endocannabinoid 60 99.98 Very High Very High Very High
dorsal root ganglion 27 99.68 Very High Very High Very High
Cannabinoid 35 99.36 Very High Very High Very High
Pain 57 99.28 Very High Very High Very High
Inflammation 32 99.28 Very High Very High Very High
cINOD 3 98.92 Very High Very High Very High
agonist 11 98.32 Very High Very High Very High
Peripheral nerve injury 4 97.60 Very High Very High Very High
Analgesic 17 96.72 Very High Very High Very High
Delta-9-tetrahydrocannabinol 2 93.92 High High
Disease Link Frequency Relevance Heat
Ganglion Cysts 28 99.20 Very High Very High Very High
INFLAMMATION 18 98.20 Very High Very High Very High
Nervous System Injury 4 97.16 Very High Very High Very High
Cognitive Disorder 2 95.92 Very High Very High Very High
Pain 44 94.76 High High
Nociception 32 89.56 High High
Anxiety Disorder 2 85.68 High High
Recurrence 1 84.48 Quite High
Hypersensitivity 9 79.16 Quite High
Inflammatory Pain 1 75.00 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Monoacylglycerol lipase (MGL) and fatty-acid amide hydrolase (FAAH) degrade the endocannabinoids 2-arachidonoylglycerol (2-AG) and anandamide (AEA), respectively.
Protein_catabolism (degrade) of FAAH associated with endocannabinoid
1) Confidence 0.97 Published 2010 Journal Pharmacol. Res. Section Abstract Doc Link 20416378 Disease Relevance 0.26 Pain Relevance 0.51
Monoacylglycerol lipase (MGL) and fatty-acid amide hydrolase (FAAH) degrade the endocannabinoids 2-arachidonoylglycerol (2-AG) and anandamide (AEA), respectively.
Protein_catabolism (degrade) of fatty-acid amide hydrolase associated with endocannabinoid
2) Confidence 0.97 Published 2010 Journal Pharmacol. Res. Section Abstract Doc Link 20416378 Disease Relevance 0.26 Pain Relevance 0.51
Fatty acid amide hydrolase (FAAH) is a membrane-bound enzyme activity that degrades neuromodulatory fatty acid amides, including oleamide and anandamide.
Protein_catabolism (degrades) of FAAH
3) Confidence 0.89 Published 1997 Journal J. Neurosci. Res. Section Abstract Doc Link 9452020 Disease Relevance 0 Pain Relevance 0.06
Fatty acid amide hydrolase (FAAH) is an integral membrane enzyme that degrades the fatty acid amide family of signaling lipids, including the endocannabinoid anandamide.
Protein_catabolism (degrades) of Fatty acid amide hydrolase associated with endocannabinoid
4) Confidence 0.88 Published 2007 Journal Biochemistry Section Abstract Doc Link 17949010 Disease Relevance 0.37 Pain Relevance 0.43
Fatty acid amide hydrolase (FAAH) is a degradative enzyme for a group of endogenous signaling lipids that includes anandamide (AEA).
Protein_catabolism (degradative) of FAAH
5) Confidence 0.88 Published 2009 Journal J. Neurosci. Section Abstract Doc Link 19321773 Disease Relevance 0.50 Pain Relevance 0.43
Fatty acid amide hydrolase (FAAH) is a degradative enzyme for a group of endogenous signaling lipids that includes anandamide (AEA).
Protein_catabolism (degradative) of Fatty acid amide hydrolase
6) Confidence 0.88 Published 2009 Journal J. Neurosci. Section Abstract Doc Link 19321773 Disease Relevance 0.50 Pain Relevance 0.43
We recently demonstrated that inhibition by URB597 of fatty acid amide hydrolase (FAAH), the main enzyme that degrades the endogenous cannabinoid N-acylethanolamine (NAE) anandamide and the endogenous non-cannabinoid NAEs oleoylethanolamide and palmitoylethanolamide, blocks nicotine-induced excitation of ventral tegmental area (VTA) dopamine (DA) neurons and DA release in the shell of the nucleus accumbens (ShNAc), as well as nicotine-induced drug self-administration, conditioned place preference and relapse in rats.
Protein_catabolism (degrades) of FAAH in ventral associated with nucleus accumbens, ventral tegmentum, dopamine, nicotine, cannabinoid and recurrence
7) Confidence 0.87 Published 2010 Journal Addict Biol Section Abstract Doc Link 20477753 Disease Relevance 0.08 Pain Relevance 0.88
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.
Protein_catabolism (degradation) of FAAH in blood associated with endocannabinoid and analgesic
8) Confidence 0.87 Published 2004 Journal Biochem. Biophys. Res. Commun. Section Abstract Doc Link 14715265 Disease Relevance 0 Pain Relevance 0.27
To address this question, we developed a peripherally restricted inhibitor (URB937) of fatty acid amide hydrolase (FAAH), the enzyme responsible for the degradation of the endocannabinoid anandamide.
Protein_catabolism (degradation) of FAAH associated with endocannabinoid
9) Confidence 0.78 Published 2010 Journal Nat. Neurosci. Section Abstract Doc Link 20852626 Disease Relevance 0.52 Pain Relevance 0.76
Fatty acid amide hydrolase (FAAH) is a serine hydrolase responsible for the degradation of anandamide, an endogenous cannabinoid agonist, and oleamide, a sleep-inducing lipid.
Protein_catabolism (degradation) of FAAH associated with cannabinoid and agonist
10) Confidence 0.70 Published 2005 Journal J. Am. Chem. Soc. Section Abstract Doc Link 16332087 Disease Relevance 0 Pain Relevance 0.18
Fatty acid amide hydrolase (FAAH) is a serine hydrolase responsible for the degradation of anandamide, an endogenous cannabinoid agonist, and oleamide, a sleep-inducing lipid.
Protein_catabolism (degradation) of Fatty acid amide hydrolase associated with cannabinoid and agonist
11) Confidence 0.70 Published 2005 Journal J. Am. Chem. Soc. Section Abstract Doc Link 16332087 Disease Relevance 0 Pain Relevance 0.18
In contrast, AM-404 (1-10 mg/kg i.p.), an inhibitor of transport of anandamide, and URB-597 (0.01-0.3 mg/kg i.p.), an inhibitor of the enzyme fatty acid amide hydrolase (FAAH) that degrades anandamide, or their combination, did not increase reinforcing efficacy of heroin at any dose tested.
Protein_catabolism (degrades) of FAAH
12) Confidence 0.64 Published 2005 Journal Neuropsychopharmacology Section Abstract Doc Link 15870833 Disease Relevance 0 Pain Relevance 0.62
Anandamide, an endocannabinoid, is degraded by the enzyme fatty acid amide hydrolase which can be inhibited by nonsteroidal anti-inflammatory drugs (NSAIDs).
Protein_catabolism (degraded) of fatty acid amide hydrolase associated with endocannabinoid, inflammation and cinod
13) Confidence 0.63 Published 2006 Journal Pain Section Abstract Doc Link 16480822 Disease Relevance 0.25 Pain Relevance 0.46
Localization of the endocannabinoid-degrading enzyme fatty acid amide hydrolase in rat dorsal root ganglion cells and its regulation after peripheral nerve injury.
Protein_catabolism (degrading) of fatty acid amide hydrolase in dorsal root ganglion associated with ganglion cysts, dorsal root ganglion, endocannabinoid, nervous system injury and peripheral nerve injury
14) Confidence 0.57 Published 2009 Journal J. Neurosci. Section Title Doc Link 19321773 Disease Relevance 0.83 Pain Relevance 0.94
URB597 is one of the best characterized covalent inhibitors of the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH).
Protein_catabolism (degrading) of FAAH associated with endocannabinoid
15) Confidence 0.36 Published 2010 Journal J. Mol. Biol. Section Abstract Doc Link 20493882 Disease Relevance 0.29 Pain Relevance 0.24
URB597 is one of the best characterized covalent inhibitors of the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH).
Protein_catabolism (degrading) of fatty acid amide hydrolase associated with endocannabinoid
16) Confidence 0.36 Published 2010 Journal J. Mol. Biol. Section Abstract Doc Link 20493882 Disease Relevance 0.29 Pain Relevance 0.24
The synthesis of anandamide is regulated by the phospholipase D, while another intracellular enzyme, the Fatty Acid Amide Hydrolase (FAAH) is responsible of its degradation, followed by the reassumption of its constituents in phospholipids [31].
Protein_catabolism (degradation) of Fatty Acid Amide Hydrolase
17) Confidence 0.32 Published 2009 Journal The Open Neurology Journal Section Body Doc Link PMC2771268 Disease Relevance 0.48 Pain Relevance 0.74
The endocannabinoid system includes: (1) at least two families of lipid signaling molecules, the N-acyl ethanolamines (e.g., anandamide) and the monoacylglycerols (e.g., 2-arachidonoyl glycerol); (2) multiple enzymes involved in the biosynthesis and degradation of these lipids, including the integral membrane enzyme fatty acid amide hydrolase; and (3) two G-protein coupled receptors, CB1 and CB2, which are primarily localized to the nervous system and immune system, respectively.
Protein_catabolism (degradation) of fatty acid amide hydrolase in immune system associated with endocannabinoid
18) Confidence 0.31 Published 2004 Journal J. Neurobiol. Section Abstract Doc Link 15362158 Disease Relevance 0.24 Pain Relevance 0.55
The endocannabinoid system includes: (1) at least two families of lipid signaling molecules, the N-acyl ethanolamines (e.g., anandamide) and the monoacylglycerols (e.g., 2-arachidonoyl glycerol); (2) multiple enzymes involved in the biosynthesis and degradation of these lipids, including the integral membrane enzyme fatty acid amide hydrolase; and (3) two G-protein coupled receptors, CB1 and CB2, which are primarily localized to the nervous system and immune system, respectively.
Protein_catabolism (degradation) of fatty acid amide hydrolase in nervous system associated with endocannabinoid
19) Confidence 0.10 Published 2004 Journal J. Neurobiol. Section Abstract Doc Link 15362158 Disease Relevance 0.24 Pain Relevance 0.55

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