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Treatment with zeocin from the beginning of the cell cycle blocked cell cycle progression in G2 phase with duplicated DNA.
In cultures treated from the beginning of the cell cycle, 30% of the cells attained the 1st CP, followed by nuclear and cellular divisions (Fig. 3D, 4E).
The cultures treated by zeocin from the beginning of the cell cycle grew slightly slower than untreated cultures (statistical difference p = 0.1), and final cell size was about 20% less (Fig. 2A).
Similarly to single treatments, the combined treatment of zeocin (8.8 µM) and caffeine (2 mM) was applied either from the beginning of the cell cycle or from the 8th h into the light period.
In the cultures treated with zeocin from the beginning of the cell cycle, DNA levels were duplicated but the timing of DNA replication was delayed compared to an untreated culture (Fig. 2D).
Zeocin (8.8 µM) was applied either from the beginning of the cell cycle (G1 phase) or at the 8th hour into the light period (G2 phase of the first DNA-division sequence – e. g. after the first S phase was completed and before nuclear division occurred) (Fig. 2E, 3E, G).
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Is it the beginning of the cell cycle of the beginning of the accumulation phase.
After 40 h from the beginning of the transfection, cells were treated with inhibitors or vehicle for 24 h.
From the beginning of the second postnatal week (P8) the density of CR cells declined progressively (Fig. 1b, c).
From the beginning of the confluent phase, mRNA expression of RUNX2, SP7, DLX5 and SPP1 was detected in DFOG cells.
Since cyclin A is active and detectable from the beginning of the S phase to the beginning of mitosis, it should theoretically label the proportion of cells that are sensitive to chemotherapeutic drugs used in our study.
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