EC Number   |
General Information |
Reference |
|---|
   3.5.1.99 | evolution |
FAAH is a member of the amidase signature family found in bacteria, archaea and eukaryotes |
720242 |
| 3.5.1.99 | evolution |
fatty acid amide hydrolase is an amidase-signature family member |
720927 |
| 3.5.1.99 | malfunction |
effects of FAAH inhibition on bladder function during urodynamics in awake rats, overview |
-, 719414 |
| 3.5.1.99 | 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 |
734439 |
| 3.5.1.99 | malfunction |
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 |
-, 719538 |
| 3.5.1.99 | malfunction |
tissue-specific changes in N-acyl ethanolamine congeners and N-acyl taurines metabolism caused by FAAH disruption in central and peripheral tissues, overview |
720176 |
| 3.5.1.99 | metabolism |
FAAH is a key enzyme in the endocannabinoid metabolism |
712466 |
| 3.5.1.99 | metabolism |
fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) are key hydrolytic enzymes of the endocannabinoid system |
733508 |
| 3.5.1.99 | metabolism |
fatty acid amide hydrolase is a key regulator of endocannabinoid-induced myocardial tissue injury |
-, 719538 |
| 3.5.1.99 | metabolism |
fatty acid amide hydrolase terminates the analgesic and anti-inflammatory effects of endocannabinoids such as anandamide |
753277 |
