作者: Rosalie Sears , Gustavo Leone , James DeGregori , Joseph R Nevins
DOI: 10.1016/S1097-2765(00)80308-1
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摘要: Abstract Various experiments have demonstrated a collaborative action of Myc and Ras, both in normal cell growth control as well during oncogenesis. We now show that Ras enhances the accumulation activity by stabilizing protein. Whereas has very short half-life when produced absence mitogenic signals, due to degradation 26S proteasome, increases markedly growth-stimulated cells. This stabilization is dependent on Ras/Raf/MAPK pathway not augmented proteasome inhibition, suggesting inhibits proteasome-dependent Myc. propose one aspect Myc–Ras collaboration an ability enhance transcriptionally active