Possible involvement of protein kinase C in mediating gastrin-induced response in rat colonic epithelium

We examined the potential role of protein kinase C in signal transduction induced by gastrin's stimulation of rat colonic epithelium. Protein synthesis ([ 35S]methionine incorporation into protein) and enzyme activity (decrease in the cytosolic activity) were measured following epithelial stimu...

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Veröffentlicht in:Peptides (New York, N.Y. : 1980) N.Y. : 1980), 1991-09, Vol.12 (5), p.925-927
Hauptverfasser: Yassin, Rihab R., Murthy, S.N.S.
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Murthy, S.N.S.
description We examined the potential role of protein kinase C in signal transduction induced by gastrin's stimulation of rat colonic epithelium. Protein synthesis ([ 35S]methionine incorporation into protein) and enzyme activity (decrease in the cytosolic activity) were measured following epithelial stimulation with gastrin. Gastrin (10 nM) increased [ 35S]methionine incorporation into protein to 265% above maintenance level. The effect of gastrin was comparable to the stimulation induced by phorbol 12-myristate, 13-acetate (PMA), a strong activator of protein kinase C. The increase in protein synthesis induced by gastrin was totally abolished by 1-(5-isoquinolinyl)-2-methylpiperazine, an inhibitor of protein kinase C activity. Gastrin also decreased the cytosolic activity of the enzyme, an index of its activation and subsequent translocation to other cellular compartments. Therefore, we conclude that gastrin may be acting through a protein kinase C mechanism.
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Protein synthesis ([ 35S]methionine incorporation into protein) and enzyme activity (decrease in the cytosolic activity) were measured following epithelial stimulation with gastrin. Gastrin (10 nM) increased [ 35S]methionine incorporation into protein to 265% above maintenance level. The effect of gastrin was comparable to the stimulation induced by phorbol 12-myristate, 13-acetate (PMA), a strong activator of protein kinase C. The increase in protein synthesis induced by gastrin was totally abolished by 1-(5-isoquinolinyl)-2-methylpiperazine, an inhibitor of protein kinase C activity. Gastrin also decreased the cytosolic activity of the enzyme, an index of its activation and subsequent translocation to other cellular compartments. Therefore, we conclude that gastrin may be acting through a protein kinase C mechanism.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>1800956</pmid><doi>10.1016/0196-9781(91)90039-R</doi><tpages>3</tpages></addata></record>
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subjects 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
Analysis of Variance
Animals
Biological and medical sciences
colon
Colon - drug effects
Colon - enzymology
Colon - metabolism
Epithelium - drug effects
Epithelium - enzymology
Epithelium - metabolism
Fundamental and applied biological sciences. Psychology
Gastrin
Gastrins - pharmacology
In Vitro Techniques
Intestine. Mesentery
Isoquinolines - pharmacology
Kinetics
Male
Methionine - metabolism
Piperazines - pharmacology
PMA
Protein Biosynthesis
Protein kinase C
Protein Kinase C - antagonists & inhibitors
Protein Kinase C - metabolism
Protein synthesis
Rats
Rats, Inbred Strains
Tetradecanoylphorbol Acetate - pharmacology
Vertebrates: digestive system
title Possible involvement of protein kinase C in mediating gastrin-induced response in rat colonic epithelium
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