scholarly journals Protein kinase C bidirectionally modulatesIhand hyperpolarization-activated cyclic nucleotide-gated (HCN) channel surface expression in hippocampal pyramidal neurons

2015 ◽  
Vol 593 (13) ◽  
pp. 2779-2792 ◽  
Author(s):  
Aaron D. Williams ◽  
Sangwook Jung ◽  
Nicholas P. Poolos
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Cyclic Nucleotide ◽  
Pyramidal Neurons ◽  
Surface Expression ◽  
Hcn Channel ◽  
Hippocampal Pyramidal Neurons ◽  
Kinase C ◽  
Channel Surface

Protein kinase C induces endocytosis of the sodium taurocholate cotransporting polypeptide

2010 ◽  
Vol 299 (2) ◽  
pp. G320-G328 ◽  
Author(s):  
Claudia Stross ◽  
Angelika Helmer ◽  
Katrin Weissenberger ◽  
Boris Görg ◽  
Verena Keitel ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Bile Salt ◽  
Fluorescent Protein ◽  
Membrane Surface ◽  
Sodium Taurocholate ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
Salt Uptake ◽  
Kinase C

Bile salts influence signaling and metabolic pathways. In hepatocytes, the sodium taurocholate cotransporting polypeptide (Ntcp) is a major determinant of intracellular bile salt levels. Short-term downregulation of Ntcp is not well characterized to date. FLAG and enhanced green fluorescent protein (EGFP) tags were cloned to the extra- and intracellular termini of Ntcp. Endocytosis of Ntcp in transfected HepG2 cells was visualized by fluorescence of EGFP, and membrane surface expression of Ntcp was quantified by flow cytometry with fluorochrome-labeled FLAG antibodies. Activation of protein kinase C (PKC) by phorbolester or thymeleatoxin an activator of Ca2+-dependent conventional PKCs (cPKCs), induced endocytosis of Ntcp, whereas the Na+-K+-ATPase remained in the plasma membrane. The PKC inhibitor BIM I and the cPKC-selective inhibitor Gö6976 abolished PMA-induced endocytosis. Because of this internalization, cell surface expression of Ntcp was reduced by 36 ± 7%, bile salt uptake was decreased by 25%, and taurolithocholate sulfate-induced cell toxicity was prevented. In conclusion, Ca2+-dependent PKCs induce vesicular retrieval of Ntcp, thereby reducing bile salt uptake. This mechanism may protect hepatocytes from toxic intracellular bile salt concentrations.

scholarly journals The activation-induced decrease in the platelet surface expression of the glycoprotein Ib-IX complex is reversible

Blood ◽  
1994 ◽  
Vol 83 (12) ◽  
pp. 3562-3573 ◽  
Author(s):  
AD Michelson ◽  
SE Benoit ◽  
MH Kroll ◽  
JM Li ◽  
MJ Rohrer ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Light Chain ◽  
Myosin Light Chain Kinase ◽  
Myosin Light Chain ◽  
Surface Expression ◽  
Platelet Surface ◽  
Kinase C ◽  
Von Willebrand ◽  
Willebrand Factor

Abstract Thrombin decreases the platelet surface expression of the glycoprotein (GP) Ib-IX complex. To determine whether this effect is reversible, flow cytometric studies were performed with GPIb-IX-specific monoclonal antibodies. In both whole blood and washed platelet systems, incubation of platelets with thrombin or a combination of adenosine diphosphate and epinephrine resulted in a maximal decrease of the platelet surface expression of GPIb-IX within 5 minutes, after which there was a time- dependent return of the platelet surface GPIb-IX complex, which was maximal by 60 minutes. Exposure of the same platelets to additional exogenous thrombin resulted in a second decrease in platelet surface GPIb-IX, followed by a second reconstitution of platelet surface GPIb- IX. Throughout these experiments there was no measurable release from the platelets of glycocalicin (a proteolytic fragment of GPIb). Experiments in which platelets were preincubated with a biotinylated GPIb-specific MoAb showed that the GPIb molecules that returned to the platelet surface were the same molecules that had been translocated to the intraplatelet pool. The GPIb molecules that returned to the platelet surface were functionally competent to bind von Willebrand factor, as determined by ristocetin-induced platelet agglutination and ristocetin-induced binding of exogenous von Willebrand factor. Inhibitors of protein kinase C and myosin light-chain kinase enhanced the reexpression of platelet surface GPIb. In summary, the activation- induced decrease in the platelet surface expression of the GPIb-IX complex is reversible. Inactivation of protein kinase C and myosin light-chain kinase are important mechanisms in the reexpression of the platelet surface GPIb-IX complex.

Differential effects of intracellular calcium elevating agents on adrenergic-stimulated cyclic nucleotide and melatonin synthesis in rat pinealocytes

1992 ◽  
Vol 70 (9) ◽  
pp. 1254-1260 ◽  
Author(s):  
Anthony K. Ho ◽  
Joshua Cheng ◽  
Marc Girard
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Cyclic Amp ◽  
Intracellular Calcium ◽  
Cyclic Nucleotide ◽  
Melatonin Synthesis ◽  
Kinase C ◽  
Mechanism Of Inhibition ◽  
Intracellular Ca

In this study, the role of elevation of intracellular Ca2+ and activation of protein kinase C on adrenergic-stimulated cyclic nucleotide accumulation and melatonin synthesis in rat pinealocytes was investigated. It was found that whereas KCl, ionomycin, and ouabain, three Ca2+-elevating agents, had a potentiating effect on adrenergic-stimulated cylic AMP response, their effects on melatonin synthesis were inhibitory. Similar inhibition was also observed when dibutyryl cyclic AMP was used to stimulate melatonin synthesis. By determining intracellular Ca2+ directly, it was found that the enhancing effects of these agents on the cyclic AMP response but not their inhibitory effects on melatonin synthesis paralleled their abilities to elevate intracellular Ca2+. In comparison, activation of protein kinase C significantly enhanced the adrenergic-stimulated cyclic AMP response and, to a lesser degree, the adrenergic-stimulated N-acetyltransferase and melatonin levels. These results indicate that (i) Ca2+-elevating agents have opposite effects on adrenergic-stimulated cyclic AMP and melatonin production; (ii) a post cyclic AMP event of importance to melatonin synthesis is inhibited by these agents; and (iii) the mechanism of inhibition may not be directly related to their effect on intracellular Ca2+.Key words: intracellular calcium, protein kinase C, melatonin, pineal gland.

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