Tunicamycin inhibits the initiation of DNA synthesis stimulated by prostaglandin F2α 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 F2α 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...

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Guardado en:
Detalles Bibliográficos
Publicado: 1991
Materias:
DNA synthesis
Lag phase
Prostaglandin F2α
Swiss 3T3 cell
Tunicamycin
insulin
prostaglandin f2 alpha
tunicamycin
animal cell
article
cell growth
dna synthesis
mouse
nonhuman
priority journal
3T3 Cells
Animal
Cell Division
Dinoprost
DNA
Glucosamine
Glycoproteins
In Vitro
Insulin
Mannose
Mice
Support, Non-U.S. Gov't
Time Factors
Animalia
Acceso en línea:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00145793_v290_n1-2_p239_Estevez
http://hdl.handle.net/20.500.12110/paper_00145793_v290_n1-2_p239_Estevez
Aporte de:
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires
Descripción
Sumario:Tunicamycin, an inhibitor of the asparagine-linked protein N-glycosylation, blocks the initiation of DNA synthesis in Swiss 3T3 cells stimulated by prostaglandin F2α 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 PGF2α stimulation. In contrast tunicamicin 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 PGF2α. © 1991.

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