◀ Back to LEP

FAAH — LEP

Text-mined interactions from Literome

Maccarrone et al., J Biol Chem 2003 : Stimulation of FAAH occurred through up-regulation of gene expression at transcriptional and translational levels and involved binding of leptin to its receptor with an apparent dissociation constant ( K ( d ) ) of 1.95 +/- 0.14 nm and maximum binding ( B ( max ) ) of 392 +/- 8 fmol x mg protein ( -1 ) ... Consistently, mutation of this site prevented FAAH activation by leptin in transient expression assays ... Taken together, these results suggest that leptin , by up-regulating the FAAH promoter through STAT3, enhances FAAH expression, thus tuning the immunomodulatory effects of anandamide
Maccarrone et al., J Biol Chem 2003 : Taken together, these results suggest that progesterone and leptin , by up-regulating the FAAH promoter at different sites, enhance FAAH expression, thus tuning the immunomodulatory effects of anandamide
Maccarrone et al., Eur J Biochem 2004 : Differential regulation of fatty acid amide hydrolase promoter in human immune cells and neuronal cells by leptin and progesterone ... Here, we extend these observations to immortalized human lymphoma U937 cells, where stimulation of FAAH by leptin ( up to approximately 300 % of the controls ) involves binding to a leptin receptor ( Kd = 2.0 +/- 0.1 nm, Bmax = 382 +/- 5 fmol.mg protein ( -1 ), apparent molecular mass of approximately 110 kDa ), and stimulation by progesterone involves an intracellular receptor of approximately 120 kDa ... Interestingly, human neuroblastoma CHP100 cells also have a leptin receptor ( approximately 110 kDa, Kd = 2.2 +/- 0.2 nm, Bmax = 339 +/- 8 fmol.mg protein ( -1 ) ), a progesterone receptor ( approximately 120 kDa ), STAT3 and Ikaros, yet their FAAH is not activated by leptin or progesterone
Gasperi et al., Neurotoxicology 2005 : Further insights into the regulation of human FAAH by progesterone and leptin implications for endogenous levels of anandamide and apoptosis of immune and neuronal cells