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Mutations involve single genes or binding sites or stretches of genome.
This similar proportion between single and multiple repeat changes differs with one of the general properties of the mutation model for bacterial VNTRs proposed by Vogler et al. [ 18], who indicated that the majority of mutations involve single repeats, although a certain percentage of events consist of multiple repeats.
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We also found some ORFs with apparent frame-shift or truncation mutations involving single neucleotide insertion or deletion.
Intrinsically resistant cells acquire this phenotype due to a spontaneous mutation involving single or multiple random steps.
8, 9 Type II disease is typified by mutations that involve single amino acid substitutions, which are more likely to lead to synthesis of a dysfunctional protein.
The most appealing initial target has been BRAF itself, as most mutations involve a single residue in the kinase domain of the protein.
More than 90% of BRAF mutations involve a single point mutation, T1799A, in codon 600 of exon 15, leading to a V600E amino acid substitution [ 9, 10].
The majority of the mutations involve a single amino acid submission at codon 12 or 13, which decreases the intrinsic guanosine triphosphatase activity and which leads to the constitutive activation of the K- ras signaling pathway.
Approximately 80% of the detected mutations involve a single substitution in exon 15 of the BRAF gene at position 600, which most commonly substitutes valine for glutamic acid (V600E), designated as BRAFV600E and resulting in permanent activation of BRAF [ 14].
All involve single base mutations: 1 in the first base, 2 in the second, and 2 in the third anticodon position.
All new mutations involved a single nucleotide.
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