In contrast, ActD (≤ 100 nM) dose - dependently
decreased cell viability and increased active p53 in the HepG2 cells.
Treatment with ActD at low doses of 3 - 30 nM for the 293 and 293T cells, and 3 - 100 nM for the HepG2 cells, for 24 and 48 hours dose - dependently
decreased cell viability (Fig. 8).
However, treatment with ActD of 30 - 300 nM for the 293 and 293T cells, and 100 and 300 nM for the HepG2 cells, for 24 and 48 hours significantly
decreased cell viability by a similar level.
Our findings confirm previously published data as treatment of Karpas 299 and SU - DHL1 cells with increasing concentrations of LY294002 led to
decreased cell viability and increased apoptosis, as determined by Annexin V staining, in a dose - dependent manner (Supplementary Fig.
Similarly, silencing of mTOR also resulted in
decreased cell viability and increased Annexin V — positive cells in comparison with control cells and with cells transfected with 4E - BP1 - specific siRNA (Fig. 6B).
High doses (≥ 30 nM) of ActD did not further
decrease cell viability or increase p53 expression.
Not exact matches
Using a zebrafish embryo xenograft model we also demonstrated that anti-CD90 monoclonal antibodies
decreased the
viability and metastatic potential of insulinoma
cells, suggesting that anti-CD90 monoclonals form a potential novel adjutant therapeutic modality.
For rare
cell populations, these losses in recovery and
viability present challenges for end users performing research on a process with potential for transfer to clinical scale by
decreasing the ability for process time and cost efficiency.
Nevertheless, we examined whether the reduction of IL - 22 production by ILC3s correlated with a
decrease in
cell viability.
Moreover, annexin V / propidium iodide staining showed that VPA only marginally
decreased the
viability of in vitro — differentiated Th1 and Th17
cells at a relatively high concentration (1 mM)(Supplemental Fig. 4A, 4B), whereas VPA readily inhibited the differentiation of Th1 and Th17
cells at a low concentration (0.2 — 0.5 mM), indicating that apoptosis induction was not the primary mechanism for Th1 and Th17
cell differentiation inhibition (28, 29).
This dichotomy points out the importance of an indirect influence on proteins whose altered function is required during carcinogenesis but are too essential to be mutated (i.e., mutation of their encoding genes could
decrease the
viability of cancer
cells).
Genetic ablation of a Na + / H + exchanger (NHE2), which is expressed in the stomach at high levels, leads to a
decrease in gastric acid secretion, along with
decreased viability of parietal
cells, severe metaplasia, and hyperplasia of gastric mucosa.