To discriminate between these two possibilities, cells were treated with hydroxyurea (HU) in order to impede fork progression.
To distinguish between these possibilities, cells were treated with Dex±iAs and ChIP analysis was done with an antibody to CARM1.
To differentiate between these possibilities, cells were inoculated with Ad-ICP0 or Ad-n212 for twelve hours, and then cells were treated with cycloheximide at the time of HSV-1 0−GFP inoculation.
Further supporting this possibility, cell death induced by IZ was not accompanied by the activation of caspases, as occurs during apoptosis.
To test this possibility, cell growth rates and biomass yield were measured in the long-term cultivation of dense algal suspensions under high irradiance.
To test this possibility, cell death and apoptosis were monitored using the clonogenic test and TUNEL staining after transition from anaerobiosis to aerobiosis.
In an effort to address this possibility, cells were treated with peptides 15D and 15K and the chemokine levels were determined by ELISA.
To assess this possibility, cells were stained on day 0 (immediately following HIV infection) with CFSE and proliferation assessed by comparing CFSE dilution between HIV-infected but untreated, and HIV-infected but TRAIL-treated cells (Fig. 2B).
To test this possibility, cells were first electroporated with free PC-Brk1, then labeled with [35S] methionine and cysteine during a pulse of 15 minutes, and chased for three hours to give enough time for Wave complex assembly.
To examine this possibility, cells were loaded with the permeable and redox-sensitive dye, DCFH-DA and ROS production was assessed in the absence or presence of 5 50 µM of either erythrodiol or uvaol.
