Furthermore, cell divisions were detected only in 6/17 APs transfected with ninein siRNA during the time-lapsed observation period, as shown in Fig. 3C.
When defects in cell division are detected, the DNA damage response prevents phase transition through the activation of cell cycle checkpoints, which induce cell cycle arrest allowing repair of damaged DNA.
In short, cell division was detected by a sharp twofold drop in total fluorescence level between consecutive images.
Only two proteins involved in plastid division were detected (Table 4).
Cell division was detected by staining T cells with 1 μM CFSE (Invitrogen) prior to activation or differentiation assays.
An additional division was detected between CQ1 and other populations in the SWP region at K = 6.
Incorrect processes, such as respiration and cell division, were detected in more than 35% of student responses and are captured by the alternative concept incorrect process.
Additionally, cell division was detected on DN1 T cells by day 13 and on P25 T cells by day 15 in the MLN.
It is worth noting that almost 10 times as many cells with endoduplicated nuclei (nuclear division without cell division) were detected in MeSC compared to SkSC after vincristine treatment.
In the duodenum, no general pathology that might have resulted from inhibition of cell division was detected, as there were no differences in crypt or villus architecture, or goblet cell density between treated and untreated mice.
