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Most retropseudogenes have undergone extensive mutational decay over evolutionary time, acquiring mutations that render them non-functional, such as large deletions and insertions (including retroelement insertions), frameshifts, and premature termination codons.
For triple combination therapy to be advantageous, most resistant cells must harbor mutations that render them resistant against two of the drugs (but not the third one).
In addition two genes of the putative ABC erythritol transport system, eryF and eryG (BOV_A805 and BOV_A806)) carry mutations that render them pseudogenes (a 2 bp deletion resulting in an premature stop codon).
It is possible that these enzymes contain mutations that render them inactive.
Methylated CpGs can undergo deamination and thereby lead to mutations that render them unable for retrotransposition [ 8, 9].
Most duplicated genes are lost due to the accumulation of mutations that render them non-functional (pseudogenization) [ 42].
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These plasmids encoded MUS81 with conservative mutations that rendered it refractory to siRNAs #9 and #10.
The two temperature-resistant mutants seem to carry suppressor mutations that rendered cells temperature-resistance and abolished L-glutamate overproduction.
The ruvA and ruvB genes were discovered by mutations that rendered the E. coli cells sensitive to UV irradiation [ 77].
For each DBRH tested, fitness gains were abolished when we introduced mutations that rendered the respective helicase domain catalytically inactive, suggesting that helicase and therefore RNA remodelling activities are essential for buffering.
Consistent with this, there was substantial phosphorylation of Ser in a human α2β2γ1 complex, and slight phosphorylation of Ser in a human α1β2γ1 complex, when they were incubated with MgATP alone; these effects were completely abolished by D157A mutations that rendered the complexes inactive, although Ser could still be phosphorylated by Akt in the inactive complex.
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