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For long-term assays, cells were exposed to 100 nM cytarabine unless indicated otherwise.
This is of course of critical importance in long-term assays especially if the cells are not continuously monitored by microscopy.
Long-term assays have also been shown to enhance detection of LTBI and to distinguish between recently acquired and remote infections [17], [18].
A likely scenario is that WWOX/WOX1 invokes a caspase-independent pathway of apoptosis initially, followed by activation of caspases during long-term assays.
Together, these results suggest that autophagy, though induced by IFN-γ activation does not target intracellular mycobacteria in these long-term assays and is most probably not the underlying mechanism of killing M. tuberculosis or BCG by IFN-γ activated macrophages.
Furthermore, incomplete MOMP correlated with cellular recovery in long-term assays.
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For the long-term assay, 85 female ICR mice were given N-methyl-N-nitrsourea solution into their uterine corpora.
We next measured the growth suppression activity of RB mutants by a short-term assay of BrdU-incorporation and a long-term assay of flat cell formation.
In the long-term assay, we used the well-established induction of senescence by RB in the RB-deficient human SAOS-2 cells.
In the long-term assay the same stimuli were applied at the beginning except for SEB that was added on day 6 to a well of non-stimulated cultured cells.
In the long-term assay, brefeldin A (10 µg/ml) was added 4 h after the second restimulation only, and cells were then cultured for an additional 12 h.
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