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Our expectations were based on the simple assumption that regulator binding at a repressor binding site, no matter its position, would always generate repression, whereas regulator binding to an activator binding site would lead to activation only if positioned upstream of the −35 site and would otherwise lead to repression.
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Pessimists fear an unstoppable dynamic that generates repression, chaos and instability – each side feeding on the other's excesses and miscalculations.
It is remarkable that TR binding at any of the three promoter regions effectively generates repression (e.g., LacI binding of L1 in F1, F3 and F5).
With regard to the main objective of these experiments, we can nevertheless conclude that Ago co-factor depletion can cause significant relief of let-7-mediated repression despite ongoing target mRNA deadenylation, indicating that deadenylation alone is not sufficient to generate full repression.
These results suggest that different miRNA combination patterns can produce coordinate action, which increases the repressive effect of miRNAs on VEGF translation, or competitive action, which failed to generate further repression of VEGF translation.
As the expression analysis cannot differentiate primary versus secondary changes associated with MeCP2, it is still possible that MeCP2 acts primarily as a repressor and that the main activation effect in the transgenic mice cerebella is a secondary change generated by repression of a primary MeCP2 target.
Subsequent cycles of activation and repression generate circadian oscillations (i.e., one peak per day) in the expression of clock proteins to determine the intrinsic timing of the molecular clock.
Meanwhile, general repression orders have been extended.
Finally, spatial repression circuits generate regulatory transitions in the expression of key genes such as FoxY, Nanos, SoxE, and Six1/2, which now are established only in the other NSM GRNs.
(130) DSB have also been shown to generate a rapid transcriptional repression in the adjacent regions, 131) and it is possible that this repressive chromatin state can sometimes be retained even after the completion of DSB repair.
This is consistent with previous microarray data obtained (Gill SS, data not published), where high doses of toxin generated a widespread repression of genes while an LD50 or lower showed a general profile favoring positive differential expression.
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