These deviations are assumed to be normally distributed with mean 0 and a within-cell variance of δ xx.
Measurements of cell-to-cell variance in protein levels were also reported by Newman et. al. [ 24].
This high level of cell-to-cell variance can be explained by adaptive mechanisms in the underlying signal networks.
Despite this cell-to-cell variance in response, clear trends in the average phosphorylation of the individual sites as function of EGFR-mCitrine expression were observed.
This is necessary to unravel mechanisms of signal crosstalk, for example in growth factor signaling, which are otherwise blurred by cell-to-cell variance.
These deviations are assumed to be normally distributed with mean 0 and a within-cell variance of δ(j / k / l ).
Assuming the baseline follow-up correlation is 0.25 and the effect size (the ratio of variance of interaction effects to within-cell variance) is 0.40, interaction effects could be tested with at least 80% power.
However, in many physiological cases the cell-to-cell variance is not only due to noise around one cellular state but also due to subpopulations which are in qualitatively distinct types of states.
As a source of intra-population variability (hereafter referred to as noise), we added stochastic noise in total protein levels mimicking natural cell-to-cell variance in protein expression (see Methods).
In Figure 1-H the cell-cell variance is modeled by a Gaussian distribution in the protein expression and different cells in a clone would then respond differently to stimulation, leading to a continuous change in the averaged response curve (see small graph in Figure 1-H).
