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In this way, phototransduction could in theory override the deleterious effect of this mutant.
Thus we mimic the effect of this mutant by increasing k2, the parameter that represents ROP activation in response to auxin.
In fact, GKAP expression was increased by coexpression of C22S/C25S-TRIM3 compared to the negative control (empty vector), suggesting a dominant negative effect of this mutant.
In contrast, the AGS3 staining was often slightly reduced in cells expressing the mutant (Figs. 3E and 4C), a phenomenon presumably due to a dominant negative effect of this mutant on endogenous USP9x.
The effect of this mutant on AMPAR and NMDAR functions was evaluated by recording simultaneously from nearby infected and uninfected CA1 neurons (similar to those presented in Figure 2).
We then selected the 100 models from F that are most consistent with the lack of a structural effect of this mutant, i.e., for which the difference between the WT and V71E Rosetta score was closest to zero.
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Hence, we speculated that the increase in the colony number in HeLa cells by ΔFHA was caused by the dominant-negative effects of this mutant upon the endogenous wild type CHFR protein [1].
The DN effects of this mutant LMP1 have been confirmed previously 12, 13.
This may reflect the apparently subtle effects of this mutant in vivo or a lack of sensitivity of the in vitro assay.
In addition, it has been shown that POR A287P does not result in any inhibition of CYP19A1 activity (25), further highlighting the differential effects of this mutant.
Unfortunately, Arboleda and colleagues did not take the opportunity to compare the effects of this mutant in vivo in Akt1-transfected or Akt3-transfected cells.
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