cAMP-dependent positive control of cyclin A2 expression during G1/S transition in primary hepatocytes
C Desdouets, GH Thoresen… - Biochemical and …, 1999 - Elsevier
C Desdouets, GH Thoresen, C Senamaud-Beaufort, T Christoffersen, C Brechot…
Biochemical and biophysical research communications, 1999•ElseviercAMP positively and negatively regulates hepatocyte proliferation but its molecular targets
are still unknown. Cyclin A2 is a major regulator of the cell cycle progression and its
synthesis is required for progression to S phase. We have investigated whether cyclin A2
and cyclin A2-associated kinase might be one of the targets for the cAMP transduction
pathway during progression of hepatocytes through G1 and G1/S. We show that stimulation
of primary cultured hepatocytes by glucagon differentially modulated the expression of G1/S …
are still unknown. Cyclin A2 is a major regulator of the cell cycle progression and its
synthesis is required for progression to S phase. We have investigated whether cyclin A2
and cyclin A2-associated kinase might be one of the targets for the cAMP transduction
pathway during progression of hepatocytes through G1 and G1/S. We show that stimulation
of primary cultured hepatocytes by glucagon differentially modulated the expression of G1/S …
cAMP positively and negatively regulates hepatocyte proliferation but its molecular targets are still unknown. Cyclin A2 is a major regulator of the cell cycle progression and its synthesis is required for progression to S phase. We have investigated whether cyclin A2 and cyclin A2-associated kinase might be one of the targets for the cAMP transduction pathway during progression of hepatocytes through G1 and G1/S. We show that stimulation of primary cultured hepatocytes by glucagon differentially modulated the expression of G1/S cyclins. Glucagon indeed upregulated cyclin A2 and cyclin A2-associated kinase while cyclin E-associated kinase was unmodified. In conclusion, our study identifies cyclin A2 as an important effector of the cAMP transduction network during hepatocyte proliferation.
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