The phrase "activated cell cycle" is correct and usable in written English.
It can be used in biological or medical contexts to describe a cell cycle that has been initiated or stimulated, often in relation to cell division or growth.
Example: "The researchers observed that the activated cell cycle in the cancer cells led to rapid proliferation."
Alternatives: "stimulated cell cycle" or "initiated cell cycle".
Together, these data indicate that the internal titration of activated cell cycle checkpoints, hormones, and developmental factors, which determine cell competence towards stemness, division, and differentiation are decisive for organ survival following IR.
One of the significant characters of gastric cancer is the abnormal activated cell cycle [ 50].
As the mechanisms underlying these clinical results, FAP-expressing fibroblasts promoted the invasiveness and activated cell cycle of a pancreatic cancer cell line in vitro.
CDV exposed normal keratinocytes displayed activated cell cycle regulation upon DNA damage signaling to allow DNA repair via homologous recombination, resulting in genomic stability and survival.
These results indicate that an activated cell cycle regulation pathway through increased expressions of CCNE1 and CDC2 is significantly associated with poor outcome on tamoxifen therapy.
Even low dose IR-induced DNA damage immediately activated cell cycle checkpoints as indicated by phosphorylation of γH2AX, ATM and Chk2 proteins in U251-NG2 positive cells (Fig. 4c).
The auxin increase was subsequent to CYCB1 1 accumulation, however, suggesting that early IR-activated cell cycle checkpoints primarily determined growth arrest and were quickly followed by changes in auxin distribution and response.
A normal mitotic index in the p53−/−shh−/− mutant retina before neurogenesis (24 hpf) is likely to result from lack of p53-activated cell cycle inhibitory gene expression, while the rescue of cell-cycle exit and normal mitotic indices in the retina during neurogenesis may be due to both lack of cell-cycle inhibitor expression and more mitoses of differentiating cells upon cell-cycle exit.
The authors concluded that blockade of the tumor-activated cell cycle pathway may be a critical mechanism for the observed antitumorigenic effects of Tan I and Tan II treatment on vasculogenesis and angiogenesis.
When satellite cells are activated, cell-cycle markers, MyoD and Myf5 transcripts are detectable.
These results indicate that the FMD-induced DNA damage activated cell-cycle checkpoints, which induced a S-phase arrest.
