◀ Back to FAS

COA3 — FAS

Text-mined interactions from Literome

Pizer et al., Cancer Res 2000 (Breast Neoplasms) : FAS inhibitors induced a rapid increase in intracellular malonyl-CoA to several fold above control levels, whereas TOFA reduced intracellular malonyl-CoA by 60 %
Lane et al., Biochem Soc Trans 2005 : Inhibitors of FAS , administered i.c.v. ( intracerebroventricularly ) to lean or obese mice, cause a rapid rise in hypothalamic malonyl-CoA level, suppression of food intake, increased fatty acid oxidation in skeletal muscle and profound weight loss
Bandyopadhyay et al., Cancer Res 2006 (Breast Neoplasms) : Collectively, our results indicate that inhibition of FAS in breast cancer cells causes accumulation of malonyl-CoA , which leads to inhibition of CPT-1 and up-regulation of ceramide and induction of the proapoptotic genes BNIP3, TRAIL, and DAPK2, resulting in apoptosis
Wolfgang et al., J Biol Chem 2006 (Weight Gain) : Fatty acid synthase (FAS) inhibitors, administered systemically or intracerebroventricularly to lean or obese mice, increase hypothalamic malonyl-CoA leading to the suppression of food intake
Lane et al., Int J Obes Relat Metab Disord 2008 : Inhibitors of FAS , administered systemically or intracerebroventricularly to mice, increase hypothalamic malony-CoA and suppress food intake
Chen et al., J Food Sci 2011 : The inhibition kinetic results showed that OCE and acetyl-CoA competitively inhibited FAS but these compounds exhibited mixed inhibition against malonyl-CoA and NADPH