Analysis of the Cell Cycle in Mouse Embryonic Stem Cells

Overexpression of SOX9 in mouse embryonic stem cells directs the immediate chondrogenic commitment

“…In fact, SOX9 interacts with other cofactors, such as L-Sox5 and Sox6 for dimerization and subsequently activates cartilage-specific marker genes more effectively (Bernard et al, 2003;Ikeda et al, 2004). mES cells exhibit the very unique distribution of cell cycle: 15% in G1, 75% in S, and 10% in G2/M, respectively, supporting their infinite proliferation potentials in vitro without differentiation under LIF signals (Savatier et al, 2002). Our data revealed the similar cell cycle pattern in mES-IRES and -SOX9 cells to the undifferentiated mES cells (Figure 3), suggesting the unique cell cycle distribution of undifferentiated mES cells might be not interfered by the integration of exogenous SOX9 gene as well as drug selection process and long-term culture even if the mild increase of G1 was observed in mES-hSOX9 cells (3-5%, respectively), compared to mES-IRES cells (Figure 3).…”

Inhibition of cyclin D expression in human breast carcinoma cells by retinoids in vitro

“…It is well known that they are involved in the normal development process. Mouse teratocarcinoma cells di erentiated into parietal endoderm-like cells upon retinoic acid treatment in vitro (Strickland et al, 1980;Sporn and Roberts, 1983;Savatier et al, 1995). Many reports demonstrated that retinoids inhibited the growth of a variety of tumors and transformed cells.…”

Inhibition of the ATR/Chk1 Pathway Induces a p38-Dependent S-phase Delay in Mouse ES Cells

“…ES cells proliferate very actively and display an unusual cell cycle distribution with a doubling time of approximately ten hours, a high proportion of cells (60 to 70%) in S phase and only about 20% of cells in G 1 . 1 These special features of ES cell cycle are reflected in their inability to undergo normal G 1 /S-checkpoint activation after DNA damage [2][3][4][5] and thus increase the relative importance of internal S-phase checkpoints for genomic stability. Both p38 kinase and the caffeine-sensitive kinases ATR and ATM are involved in cell cycle regulation.…”