Cycling epithelial cells were shown to reversibly arrest in late G1 phase following treatment with transforming growth factor β1. Associated with this G1-S phase arrest was a decrease in the synthesis and histone H1 kinase activity of p34(cdc2). Transforming growth factor β1 did not reduce p34(cdc2) levels by modulating the turnover of newly synthesized p34(cdc2). The decrease in p34(cdc2) synthesis preceded any detectable effect on DNA synthesis. Moreover, the action of transforming growth factor β1 was regulated in a cell cycle-specific manner; epithelial cells were sensitive to transforming growth factor β1 only during the G1 phase. The results suggest that p34(cdc2) might be a useful biochemical marker for investigating the mechanism(s) of transforming growth factor β1 signaling.
|Original language||English (US)|
|Number of pages||8|
|Journal||Cell Growth and Differentiation|
|State||Published - Jan 1 1994|
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology