Tunicamycin inhibits the initiation of DNA synthesis stimulated by prostaglandin F2 alpha in Swiss mouse 3T3 cells.
Tunicamycin, an inhibitor of the asparagine-linked protein N-glycosylation, blocks the initiation of DNA synthesis in Swiss 3T3 cells stimulated by prostaglandin F2 alpha alone or with insulin. This effect is exerted only when tunicamycin is added from 0 to 8 h after stimulation and it decreases the rate of entry into S phase. Blocking of labeled sugar incorporation to proteins occurs regardless of the time of PGF2 alpha stimulation. In contrast tunicamycin does not inhibit protein synthesis. These results suggest that N-glycoprotein synthesis early during the prereplicative phase is an important event controlling the mitogenic action of PGF2 alpha.
Instituto de Investigaciones en Ingeniería Genética y Biología Molecular (INGEBI), Buenos Aires, Argentina.
A G
AG
Estevez
G
G
Calamante
M
M
Goin
L
L
Jimenez de Asua
D016475:3T3 Cells; D000818:Animals; D002455:Cell Division / Q000187:drug effects*; D004247:DNA / Q000096:biosynthesis; D015237:Dinoprost / Q000037:antagonists & inhibitors*; D005944:Glucosamine / Q000378:metabolism; D006023:Glycoproteins / Q000502:physiology*; D066298:In Vitro Techniques; D007328:Insulin / Q000494:pharmacology; D008358:Mannose / Q000378:metabolism; D051379:Mice; D013997:Time Factors; D014415:Tunicamycin / Q000494:pharmacology*
D006023:Glycoproteins; D007328:Insulin; D014415:Tunicamycin; D004247:DNA; D015237:Dinoprost; D005944:Glucosamine; D008358:Mannose