To evaluate global mRNA translation in activated B cells undergoing a DNA damage response we used etoposide, a topoisomerase II inhibitor that induces DNA double-strand breaks.
(b) A decrease in culture temperature: for the dark-grey response we used a PI controller during the 37 °C phase to achieve the desired sfGFP fluorescence.
For the dark-grey response we used a PI controller during the M9 phase, and switched it off after the shift, keeping the light input constant at the pre-shift level.
For the dark-grey response we used a PI controller during the first 5 h, and switched it off after the perturbation, keeping the light input constant at the reduced level.
To further confirm a role of KRAS mutation status in PTPRS KO-mediated modulation of EGFR phosphorylation response, we used isogenic cell pairs HCT116 (KRAS G13D/+) vs HCT116 with and without PTPRS expression.
To increase the immune response, we used a new approach based on peptide nanoparticles, which are designed to mimic an icosahedral virus capsid and allow the repetitive, ordered display of a specific epitope on their surface.
In the regime of linear response, we used an alternative approach for estimation of sensitivity by stimulating the hair cell model with broadband Gaussian noise with small variance, so that the model operated in the linear response regime.
To assess a slightly longer physiological response, we used a before-after control design.
To analyse this whole-cell response we used the integrated Lew-Bookchin red cell model [34].
To avoid making any assumptions about the shape of the RT-related response, we used an empirical estimation approach.
In order to further explore the effect of cortisol dynamics on target cell response we used an unbiased strategy of expression gene profiling.
