Treatment of Caco-2 cells with cholera toxin inhibits the activity of the H+/peptide cotransporter. The effect of cholera toxin is mimicked by E. coli heat-labile enterotoxin, forskolin and isobutylmethylxanthine and is associated with an increase in cAMP levels in the cells. The inhibition is due to a decrease in the maximal velocity of the transport system. Inhibitors of protein kinase A and protein kinase C block the effect of cholera toxin. Interestingly, the H+/peptide cotransporter in Caco-2 cells does not possess any putative site for phosphorylation by protein kinase A but does possess sites for phosphorylation by protein kinase C. It appears that the cAMP-dependent inhibition of the H+/peptide cotransporter in Caco-2 cells is mediated through activation Of protein kinase C.
|Original language||English (US)|
|Number of pages||5|
|Journal||Biochemical and Biophysical Research Communications|
|Publication status||Published - Jan 17 1996|
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology