A glucagon fragment is responsible for the inhibition of the liver Ca2+ pump by glucagon View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1987-02

AUTHORS

Ariane Mallat, Catherine Pavoine, Michel Dufour, Sophie Lotersztajn, Dominique Bataille, Françoise Pecker

ABSTRACT

Glucagon specifically inhibits the Ca2+ pump in liver plasma membranes independently of adenylate cyclase activation. However, this inhibition is only observed at high concentrations of glucagon (Ki = 0.7 microM). Moreover, in the presence of bacitracin, an inhibitor of glucagon degradation, the Ca2+ pump is no longer sensitive to glucagon. These findings suggest that a fragment of glucagon might be the true effector of the liver Ca2+ pump. Pairs of basic amino acids are recognized as potential cleavage sites in post-translational processing of peptide hormones. The glucagon molecule includes a dibasic doublet (Arg 17-Arg 18). Therefore, we have examined the action of glucagon(19-29) on the liver Ca2+ pump. This peptide was obtained from glucagon by tryptic cleavage and separated by reverse-phase high-performance liquid chromatography. We found that glucagon(19-29), which is totally ineffective in activating adenylate cyclase, inhibited both the Ca2+-activated and Mg2+-dependent ATPase activity [Ca2+-Mg2+) ATPase) and Ca2+ transport in liver plasma membranes with an efficiency 1,000-fold higher than that of glucagon. Glucagon(1-21) was completely inactive; glucagon(18-29) and glucagon(22-29) acted only as partial agonists of glucagon(19-29). These results indicate that glucagon(19-29), obtained by proteolytic cleavage of glucagon, is likely to be the active peptide involved in the inhibition of the liver Ca2+ pump. We suggest that glucagon may be a precursor of at least one biologically active peptide. More... »

PAGES

620

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/325620a0

DOI

http://dx.doi.org/10.1038/325620a0

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1050143907

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/2949156


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