环磷酸腺苷对人肠上皮细胞系Caco-2中H⁺/肽共转运体的抑制作用。

Inhibition of the H+/peptide cotransporter in the human intestinal cell line Caco-2 by cyclic AMP.

作者信息

Muller U, Brandsch M, Prasad P D, Fei Y J, Ganapathy V, Leibach F H

机构信息

Department of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta 30912-2100, USA.

出版信息

Biochem Biophys Res Commun. 1996 Jan 17;218(2):461-5. doi: 10.1006/bbrc.1996.0082.

DOI:10.1006/bbrc.1996.0082

PMID:8561778

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.

摘要

用霍乱毒素处理Caco-2细胞会抑制H⁺/肽共转运体的活性。大肠杆菌不耐热肠毒素、福斯可林和异丁基甲基黄嘌呤可模拟霍乱毒素的作用，且这与细胞内cAMP水平升高有关。这种抑制作用是由于转运系统的最大速度降低。蛋白激酶A和蛋白激酶C的抑制剂可阻断霍乱毒素的作用。有趣的是，Caco-2细胞中的H⁺/肽共转运体不具有任何蛋白激酶A磷酸化的假定位点，但具有蛋白激酶C磷酸化的位点。看来，Caco-2细胞中H⁺/肽共转运体的cAMP依赖性抑制是通过蛋白激酶C的激活介导的。