Abstract
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) |
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Pages (from-to) | 461-465 |
Number of pages | 5 |
Journal | Biochemical and Biophysical Research Communications |
Volume | 218 |
Issue number | 2 |
DOIs | |
State | Published - Jan 17 1996 |
ASJC Scopus subject areas
- Biophysics
- Biochemistry
- Molecular Biology
- Cell Biology