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By contrast, BET bromodomain inhibitors may induce p21Cip1 levels, thus blocking cells at the G1/S transition.
These results indicate that only at higher concentrations, BPT tends to act as a Cdk4 inhibitor blocking cells at the G0/G1 phase.
Experimentally, statins can stop cell growth by blocking cells at the G1 or G2/M stages, or induce apoptosis in several cancer cell types [ 20].
These results show that Znf179 has a role in inhibiting cell cycle progression, particularly in blocking cells at the G0/G1-phase, and promotes neuronal differentiation.
However, deletion of both genes dramatically impaired proliferation in multiple cell types by blocking cells at the G1 to S phase transition [ 6, 7].
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These two treatments efficiently blocked cells at the beginning of S phase.
For investigating the effects of DNA-damaging drugs on the cell cycle progression, we incubated cells with 100 n M CPT11, a compound known to block cells at the S phase.
However, it profoundly blocks cells at the G2/M phase at comparatively low concentrations.
Part of the mechanism by which p53 blocks cells at the G2 checkpoint involves inhibition of Cdc2, the cyclin-dependent kinase required to enter mitosis.
In contrast to agents like nocodazole, which block cells at the G2/M transition, neither silvestrol nor HHT caused Bax −/− Bak −/− cells to accumulate at any specific stage of the cell cycle (Supplementary Figure 7c) when protein synthesis and cell proliferation were inhibited by 95%.
After blocking, cells were incubated at 4°C overnight with the anti-cleaved caspapse-3 antibody (Cell signaling, Danvers, MA).
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