3.5.1.99: fatty acid amide hydrolase
This is an abbreviated version!
For detailed information about fatty acid amide hydrolase, go to the full flat file.
Word Map on EC 3.5.1.99
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3.5.1.99
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endocannabinoids
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cannabinoids
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pain
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lipase
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agonist
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monoacylglycerol
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2-arachidonoylglycerol
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anxiety
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analgesic
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cannabis
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n-acylethanolamines
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vanilloid
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2-arachidonoyl
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ethanolamide
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palmitoylethanolamide
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carbamate
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rimonabant
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hyperalgesia
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reward
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tone
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nociceptive
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cannabimimetic
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n-arachidonoylethanolamine
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marijuana
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anxiolytic
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nape-pld
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antinociceptive
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oleoylethanolamide
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emotional
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neuropathic
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delta9-tetrahydrocannabinol
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amidase
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amygdalar
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medicine
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catalepsy
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pharmacology
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anti-allodynic
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anxiolytic-like
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monoglyceride
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cannabidiol
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psychoactive
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sleep-inducing
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phytocannabinoids
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anxiety-like
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arachidonyl
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monoacyl
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capsazepine
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aversive
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tetrahydrocannabinol
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drug development
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anti-hyperalgesic
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neuromodulatory
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fluorophosphonate
- 3.5.1.99
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endocannabinoids
- cannabinoids
- pain
- lipase
- agonist
- monoacylglycerol
- 2-arachidonoylglycerol
-
anxiety
-
analgesic
- cannabis
- n-acylethanolamines
-
vanilloid
-
2-arachidonoyl
- ethanolamide
- palmitoylethanolamide
- carbamate
-
rimonabant
- hyperalgesia
-
reward
-
tone
-
nociceptive
-
cannabimimetic
- n-arachidonoylethanolamine
- marijuana
-
anxiolytic
- nape-pld
-
antinociceptive
- oleoylethanolamide
-
emotional
-
neuropathic
- delta9-tetrahydrocannabinol
- amidase
-
amygdalar
- medicine
- catalepsy
- pharmacology
-
anti-allodynic
-
anxiolytic-like
- monoglyceride
- cannabidiol
-
psychoactive
-
sleep-inducing
-
phytocannabinoids
-
anxiety-like
-
arachidonyl
-
monoacyl
-
capsazepine
-
aversive
- tetrahydrocannabinol
- drug development
-
anti-hyperalgesic
-
neuromodulatory
- fluorophosphonate
Reaction
Synonyms
AAH, anandamide amidohydrolase, AtFAAH, endocannabinoid-degrading enzyme, FA amide hydrolase, FAAH, FAAH-1, FAAH-2, fatty acid amide hydrolase, fatty-acid amide hydrolase, hFAAH, oleamide hydrolase
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General Information
General Information on EC 3.5.1.99 - fatty acid amide hydrolase
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evolution
malfunction
metabolism
physiological function
additional information
FAAH is a member of the amidase signature family found in bacteria, archaea and eukaryotes
evolution
fatty acid amide hydrolase is an amidase-signature family member
evolution
fatty acid amide hydrolase is an amidase-signature family member
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effects of FAAH inhibition on bladder function during urodynamics in awake rats, overview
malfunction
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genetic deletion of FAAH is associated with enhanced acute doxorubicin-induced myocardial cell death and decreased survival, mechanism of the doxorubicin-induced myocardial cell death in FAAH+/+ and FAAH-/- mice, overview
malfunction
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tissue-specific changes in N-acyl ethanolamine congeners and N-acyl taurines metabolism caused by FAAH disruption in central and peripheral tissues, overview
malfunction
enzyme inhibition and deficiency causes increased central and peripheral neuronal levels of anandamide and other FAAs producing physiological effects including analgesia, apoptosis in various cancer cells, 12-14 modulation of memory processes, neuroprotection, epilepsy, feeding, and prevention of neurotoxicity of the human amyloid-beta peptide in Alzheimer's disease. Also anti-depressant, anxiolytic, antiinflammatory, anti-hypertensive, gastrointestinal and sleep-inducing effects are observed
malfunction
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effects of FAAH inhibition on bladder function during urodynamics in awake rats, overview
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malfunction
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genetic deletion of FAAH is associated with enhanced acute doxorubicin-induced myocardial cell death and decreased survival, mechanism of the doxorubicin-induced myocardial cell death in FAAH+/+ and FAAH-/- mice, overview
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metabolism
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fatty acid amide hydrolase is a key regulator of endocannabinoid-induced myocardial tissue injury
metabolism
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fatty acid amide hydrolase is a key regulator of endocannabinoid-induced myocardial tissue injury
metabolism
fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) are key hydrolytic enzymes of the endocannabinoid system
metabolism
fatty acid amide hydrolase terminates the analgesic and anti-inflammatory effects of endocannabinoids such as anandamide
metabolism
the enzyme has a key role in the control of the cannabinoid signaling, through the hydrolysis of the endocannabinoids anandamide and in some tissues 2-arachidonoylglycerol
metabolism
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the enzyme is involved in many human diseases, particularly cancer, pain and inflammation as well as neurological, metabolic and cardiovascular disorders
metabolism
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fatty acid amide hydrolase is a key regulator of endocannabinoid-induced myocardial tissue injury
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FAAH is a degradative enzyme for a group of endogenous signaling lipids that includes anandamide, that acts as an endocannabinoid and an endovanilloid by activating cannabinoid and vanilloid type 1 transient receptor potential,TRPV1, receptors, respectively, on dorsal root ganglion sensory neurons. Inhibition of FAAH activity increases anandamide concentrations in nervous tissue and reduces sensory hypersensitivity in animal pain models
physiological function
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FAAH is the chief catabolic enzyme regulating the endogenous cannabinoid N-arachidonoylethanolamine, i.e. anandamide
physiological function
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FAAH is the key hydrolytic enzyme for the endogenous cannabinoid receptor ligand anandamide
physiological function
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genetic or pharmacological ablation of FAAH promotes analgesia and anxiolytic effects without disrupting motor coordination
physiological function
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importance of FAAH in controlling endogenous anandamide levels in the brain and consequently the importance of FAAH as a regulatory enzyme for key physiological functions. FAAH is one of the main enzymes responsible for terminating the signaling of endocannabinoids in the brain, it has a role in neuropsychiatric disorders
physiological function
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endocannabinoid-degrading enzyme fatty acid amide hydrolase. FAAH substrates in the urinary bladder act via local CB2-mediated signals
physiological function
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endocannabinoid-degrading enzyme fatty acid amide hydrolase. FAAH substrates in the urinary bladder act via local CB2-mediated signals
physiological function
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endocannabinoid-degrading enzyme fatty acid amide hydrolase. FAAH substrates in the urinary bladder act via local CB2-mediated signals
physiological function
fatty acid amide hydrolase degrades lipid signaling molecules such as the endogenous cannabinoids anandamide, i.e. N-arachidonyl ethanolamine, and the sleep-inducing substance oleamide, i.e. cis-9-octadecenamide
physiological function
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fatty acid amide hydrolase is a key regulator of endocannabinoid-induced myocardial tissue injury
physiological function
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fatty acid amide hydrolase is a key regulator of endocannabinoid-induced myocardial tissue injury
physiological function
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fatty acid amide hydrolase is the principal enzyme responsible for anandamide hydrolysis in mammalian tissues and regulates amidated lipid transmitters, including the endocannabinoid anandamide and its N-acyl ethanolamine congeners and transient receptor potential channel agonists N-acyl taurines, in a tissue-specific manner, overview
physiological function
the enzyme degrades and inactivates members of the fatty acid amide family of endogenous signaling lipids, including anandamide and oleamide. Anandamide binds and activates the CB1 and CB2 cannabinoid receptors, the molecular targets of plant-derived (-)-DELTA9-terahydrocannabinol, while oleamide induces physiological sleep and modulates serotonergic systems and GABAergic transmission
physiological function
the enzyme degrades and inactivates members of the fatty acid amide family of endogenous signaling lipids, including anandamide and oleamide. Anandamide binds and activates the CB1 and CB2 cannabinoid receptors, the molecular targets of plant-derived (?)-DELTA9-terahydrocannabinol, while oleamide induces physiological sleep and modulates serotonergic systems and GABAergic transmission
physiological function
primary catabolic enzyme for anandamide, an endogenous cannabinoid
physiological function
primary catabolic enzyme for anandamide, an endogenous cannabinoid
physiological function
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terminates the anti-inflammatory effects of endocannabinoids
physiological function
the enzyme plays a key role in controlling endogenous levels of endocannabinoids
physiological function
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endocannabinoid-degrading enzyme fatty acid amide hydrolase. FAAH substrates in the urinary bladder act via local CB2-mediated signals
-
physiological function
-
fatty acid amide hydrolase is a key regulator of endocannabinoid-induced myocardial tissue injury
-
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anandamide induces enhanced cell death in human cardiomyocytes pretreated by FAAH inhibitor, and enhances sensitivity to reactive oxygen species generation in inflammatory cells of FAAH knockouts
additional information
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anandamide induces enhanced cell death in human cardiomyocytes pretreated by FAAH inhibitor, and enhances sensitivity to reactive oxygen species generation in inflammatory cells of FAAH knockouts, it triggers concentration-dependent respiratory burst (ROS generation) in neutrophil granulocytes isolated from FAAH+/+ mice
additional information
overexpression of fatty acid amide hydrolase induces early flowering in Arabidopsis thaliana. The FLOWERING LOCUST gene, which plays a major role in regulating flowering time, and one target MADS box transcription factor, SEPATALLA3 (SEP3), are elevated in AtFAAH overexpressors, that also show enhanced NAE hydrolase activity. The early flowering phenotype plants have lower endogenous N-acylethanolamines, NAE, levels in leaves compared to wild-type prior to flowering. The number of rosette leaves and rosette diameter is not affected by altered AtFAAH expression
additional information
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overexpression of fatty acid amide hydrolase induces early flowering in Arabidopsis thaliana. The FLOWERING LOCUST gene, which plays a major role in regulating flowering time, and one target MADS box transcription factor, SEPATALLA3 (SEP3), are elevated in AtFAAH overexpressors, that also show enhanced NAE hydrolase activity. The early flowering phenotype plants have lower endogenous N-acylethanolamines, NAE, levels in leaves compared to wild-type prior to flowering. The number of rosette leaves and rosette diameter is not affected by altered AtFAAH expression
additional information
the active site is located in the center cavity defined by an atypical Ser-Ser-Lys catalytic triad which comprises the catalytic nucleophile residue Ser241 along with residues Ser217 and Lys142
additional information
the active site of FAAH is characterized by an atypical catalytic triad, consisting of Ser241-Ser217-Ly142, which is capable of hydrolyzing amide and ester bonds at similar rates
additional information
the active site of FAAH is characterized by an atypical catalytic triad, consisting of Ser241-Ser217-Ly142, which is capable of hydrolyzing amide and ester bonds at similar rates
additional information
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the active site of FAAH is characterized by an atypical catalytic triad, consisting of Ser241-Ser217-Ly142, which is capable of hydrolyzing amide and ester bonds at similar rates
additional information
the mammalian enzyme is in the amidase signature (AS) family bearing the unusual Ser-Ser-Lys catalytic triad
additional information
the mammalian enzyme is in the amidase signature (AS) family bearing the unusual Ser-Ser-Lys catalytic triad
additional information
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the mammalian enzyme is in the amidase signature (AS) family bearing the unusual Ser-Ser-Lys catalytic triad
additional information
-
the active site of FAAH is characterized by an atypical catalytic triad, consisting of Ser241-Ser217-Ly142, which is capable of hydrolyzing amide and ester bonds at similar rates
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additional information
-
anandamide induces enhanced cell death in human cardiomyocytes pretreated by FAAH inhibitor, and enhances sensitivity to reactive oxygen species generation in inflammatory cells of FAAH knockouts, it triggers concentration-dependent respiratory burst (ROS generation) in neutrophil granulocytes isolated from FAAH+/+ mice
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