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These two mutations led to a marked decrease expression of the mutated receptors on the cell surface compared to the wild-type TSHR (set at 100%), 74.6% for A623V and 86.4% for I691F respectively (Table 1, Figure 3B).
The rare genetic mutations led to an overproduction of amyloid, it turned out, the abnormal protein in those plaques.
Multiple parallelism in nonsynonymous mutations led to little or no improvement in various indices upon inclusion of amino acid sequences.
Most mutations in MYO7A gene caused USH1B, whereas only a few reported mutations led to DFNB2 and DFNA11.
Initial mutations led to slower growth — a finding that suggests bacteria adapting to the antibiotic aren't able to grow at optimal speed while developing mutations.
Initial mutations led to slower growth a finding that suggests bacteria adapting to the antibiotic aren't able to grow at optimal speed while developing mutations.
Reversion of such mutations led to a complete loss of binding to the target molecule, suggesting that they are critical for the recognition of human IgG4.
These mutations led to a marked decrease in the overall thermodynamic stability of the evolved KE07s and in the configurational stability of their active sites.
Upon re-engineering in C. glutamicum Δppc Δpyc, the identified mutations led to diminished ICD activities and activated the glyoxylate shunt replenishing oxaloacetate required for growth.
It had long been known that the asymmetrical appearance of a creature was directly linked to the amount of mutation in its genome, so that more mutations led to more "fluctuating asymmetry".
While the gene responsible for cystic fibrosis was identified in 1989, it took many years to figure out exactly how mutations led to the disease and even longer to figure out how to counteract the mutations.
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