INT102573

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Context Info
Confidence 0.80
First Reported 2002
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 8
Total Number 8
Disease Relevance 2.89
Pain Relevance 3.52

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
CB1 2
neuronal 1
Faah (Mus musculus)
Pain Link Frequency Relevance Heat
Endocannabinoid 153 100.00 Very High Very High Very High
addiction 9 99.12 Very High Very High Very High
Cannabinoid 63 97.26 Very High Very High Very High
Antinociceptive 1 97.16 Very High Very High Very High
Cannabinoid receptor 24 94.84 High High
agonist 64 93.60 High High
Inflammation 18 93.08 High High
depression 203 92.96 High High
Multiple sclerosis 10 88.72 High High
cytokine 3 87.20 High High
Disease Link Frequency Relevance Heat
Targeted Disruption 59 98.36 Very High Very High Very High
Neurodegenerative Disease 113 95.60 Very High Very High Very High
INFLAMMATION 17 93.08 High High
Depression 221 92.96 High High
Demyelinating Disease 11 88.72 High High
Schizophrenia 11 85.08 High High
Systemic Lupus Erythematosus 1 84.84 Quite High
Arthritis 2 83.60 Quite High
Cancer 4 82.88 Quite High
Disease 22 82.76 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
CD1 mice lacking the CB1 receptors ("knockout" [KO] mutants) were compared with wildtype (WT) littermates for their ability to degrade AEA through an AEA membrane transporter (AMT) and an AEA hydrolase (fatty acid amide hydrolase, FAAH).
Protein_catabolism (degrade) of fatty acid amide hydrolase in CB1 associated with targeted disruption
1) Confidence 0.80 Published 2002 Journal Eur. J. Neurosci. Section Abstract Doc Link 11982628 Disease Relevance 0.17 Pain Relevance 0.29
These changes were not due to differences in the expression of the degradation enzymes, fatty acid amide hydrolase and monoacylglycerol lipase, or of biosynthetic enzymes, diacylglycerol lipase-alpha and N-acylphosphatidylethanolamine phospholipase-D at this time (60 days).
Protein_catabolism (degradation) of fatty acid amide hydrolase
2) Confidence 0.78 Published 2008 Journal Eur. J. Neurosci. Section Abstract Doc Link 18657182 Disease Relevance 0.61 Pain Relevance 0.81
Many constituents of the endogenous cannabinoid system like the CB1 and CB2 receptors and their endogenous ligands Anandamide (AEA) and 2-arachidonylglycerol (2-AG) as well as the AEA-degrading enzyme fatty acid amide hydrolase (FAAH) and the 2-AG synthesizing enzyme diacylglycerol lipases are found in neuronal developmental and adult neurogenesis [20-22].
Protein_catabolism (degrading) of fatty acid amide hydrolase in neuronal associated with cannabinoid and neurodegenerative disease
3) Confidence 0.45 Published 2010 Journal Cell Commun Signal Section Body Doc Link PMC2898685 Disease Relevance 0.73 Pain Relevance 0.36
The degradation of endocannabinoid is achieved by means of two specific enzymes: the fatty acid amide hydrolase (FAAH) [51] and the monoacylglyceride lipase (MAGL) enzymes [52].
Protein_catabolism (degradation) of fatty acid amide hydrolase associated with endocannabinoid
4) Confidence 0.44 Published 2007 Journal Clin Pract Epidemiol Ment Health Section Body Doc Link PMC2169225 Disease Relevance 0 Pain Relevance 0.59
In contrast, blocking anandamide degradation (using the FAAH inhibitor URB597) had no effect.
Protein_catabolism (degradation) of FAAH
5) Confidence 0.39 Published 2007 Journal PLoS ONE Section Body Doc Link PMC1933592 Disease Relevance 0.26 Pain Relevance 0.16
FAAH degrades anandamide, whereas the MAGL degrades 2-AG.
Protein_catabolism (degrades) of FAAH
6) Confidence 0.39 Published 2007 Journal Clin Pract Epidemiol Ment Health Section Body Doc Link PMC2169225 Disease Relevance 0.11 Pain Relevance 0.58
CD1 mice lacking the CB1 receptors ("knockout" [KO] mutants) were compared with wildtype (WT) littermates for their ability to degrade AEA through an AEA membrane transporter (AMT) and an AEA hydrolase (fatty acid amide hydrolase, FAAH).
Protein_catabolism (degrade) of FAAH in CB1 associated with targeted disruption
7) Confidence 0.35 Published 2002 Journal Eur. J. Neurosci. Section Abstract Doc Link 11982628 Disease Relevance 0.17 Pain Relevance 0.29
3'-carbamoylbiphenyl-3-yl cyclohexylcarbamate (URB 597), a potent and systemically active inhibitor of FAAH (the enzyme responsible for anandamide degradation) was recently shown to directly gate TRPA1 and is being pursued as an antinociceptive drug [150].


Protein_catabolism (degradation) of FAAH associated with antinociceptive
8) Confidence 0.22 Published 2008 Journal Current Neuropharmacology Section Body Doc Link PMC2645548 Disease Relevance 0.84 Pain Relevance 0.44

General Comments

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