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N-arachidonoyl ethanolamine and 2-arachidonoyl glycerol hydrolyzing enzymes, FAAH and MAGL (show MGLL ELISA Kits), and the CB1 (show CNR1 ELISA Kits) receptor link the endocannabinoid system to broader lipid signaling networks in contrasting ways, potentially altering neurotransmission and behavior independently of cannabinoid receptor signaling.
Both inhibitors reduced several markers of macrophage activation, such as mRNA expression of inflammatory mediators, as well as cytokine and prostaglandin production, with however some differences between FAAH and NAAA (show NAAA ELISA Kits) inhibition. Our results support an important role for inhibition of NAE hydrolysis and NAAA (show NAAA ELISA Kits) inhibition in particular in controlling macrophage activation, and thus inflammation.
Inactivation of FAAH, the main degrading enzyme of anandamide and similar endocannabinoids, could lead to an increased decidual endocannabinoid tone with embryotoxic effects.
genetic deletion of FAAH may predispose animals to increased sensitivity to certain types of pain.
Impaired neurogenesis by HIV-1-Gp120 (show ITIH4 ELISA Kits) is rescued by genetic deletion of fatty acid amide hydrolase enzyme
Study identified FAAH as a novel player in the pathogenesis of lupus
Basal concentrations of anandamide was greater, and the severity of cystitis was reduced FAAH KO mice. Cystitis-associated increased peripheral sensitivity and enhanced bladder activity were attenuated in FAAH KO mice.
in FAAH(-/-) animals the number of microglia and the ratio of activated microglia and IL-1beta (show IL1B ELISA Kits) level were already higher in young animals
Results demonstrate that the supra-spinally-located FAAH enzyme is necessary for the analgesic action of paracetamol.
Data suggest that multitarget FAAH/Cox (show CPOX ELISA Kits) blockade may provide a transformative approach to inflammatory bowel disease (IBD) and other pathologies in which fatty acid amide hydrolase/cyclooxygenases (FAAH, Cox-1 (show PTGS1 ELISA Kits), and Cox-2 (show COX2 ELISA Kits)) are overactive.
High FAAH expression is associated with lung neoplasms.
study demonstrates a dose-dependent relationship between chronic cannabis use and reported sleep quality, independent of abstinence length. Furthermore, it provides novel evidence that depressive symptoms mediate the relationship between FAAH genotype and sleep quality in humans.
FAAH was significantly associated with DSM-5 cannabis use disorder group count (DSM-5 CUD) using a gene-based test (p = 0.0035). This association survived Bonferroni correction for multiple testing at p < 0.004. Post hoc analyses suggested this association was driven by two common (minor allele frequency >5%) SNPs in moderate linkage disequilibrium, rs324420 and rs4141964, at p = 0.0014 and p = 0.0023, respectively.
We first report loss-of-function mutations in DGAT2 (show DGAT2 ELISA Kits) and FAAH in one obese subject, which may interact with each other to affect the adiposity penetrance, providing a model of genetic interaction associated with human obesity.
This study suggests that interactions between anandamide and CRF1 represent a fundamental molecular mechanism regulating amygdala function and anxiety.
In cannabis users, fatty acid amide hydrolase binding was significantly lower across the brain regions examined than in matched control subjects. Lower binding was negatively correlated with cannabinoid concentrations in blood and urine and was associated with higher trait impulsiveness.
We investigated the relationship between variation in the CNR1 (show CNR1 ELISA Kits), CNR2 (show CNR2 ELISA Kits), and FAAH genes and change in primary anxiety disorder severity. Five SNPs were nominally associated with a poorer treatment response (rs806365 [CNR1 (show CNR1 ELISA Kits)]; rs2501431 [CNR2 (show CNR2 ELISA Kits)]; rs2070956 [CNR2 (show CNR2 ELISA Kits)]; rs7769940 [CNR1 (show CNR1 ELISA Kits)]; rs2209172 [FAAH]) and one with a more favorable response (rs6928813 [CNR1 (show CNR1 ELISA Kits)]).
the presence and differential distribution of fatty acid amide hydrolase (FAAH) and monoglyceride lipase (MGLL (show MGLL ELISA Kits)) in relation to CB1 (show CNR1 ELISA Kits) during the maturation of human oocytes, was investigated.
fatty acid amide hydrolase inhibition exerts cutaneous anti-inflammatory effects
In transgenic mice, a direct involvement of the human FAAH C385A SNP was associated with alcohol "binge" drinking.
AtFAAH is one, but not the only, modulator of endogenous N-Acylethanolamines (NAE) levels in plants, and that NAE depletion likely participates in the regulation of plant growth [fatty acid amide hydrolase] [AtFAAH]
Overexpression of AtFAAH inhibits innate immunity against Pseudomonas syringae in Arabidopsis, and plants had lower amounts of jasmonic acid, abscisic acid, and salicylic acid.
AtFAAH influences plant growth and interacts with ABA signaling and plant defense through distinctly different mechanisms
This gene encodes a protein that is responsible for the hydrolysis of a number of primary and secondary fatty acid amides, including the neuromodulatory compounds anandamide and oleamide.
fatty-acid amide hydrolase 1
, fatty acid amide hydrolase
, hypothetical protein LOC569067
, fatty-acid amide hydrolase
, fatty-acid amide hydrolase 1-like
, fatty acid amide hydrolase, gene 3
, oleamide hydrolase 1
, fatty acid alpha-hydroxylase
, fatty acid hydroxylase domain containing 1
, anandamide amidohydrolase 1
, amide hydrolase
, fatty acid amide hydrolase protein