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Approximately 2000 mutations, most of which are disease relevant, have been identified in the CFTR gene and then categorized in six different classes according to their functional impact [5].
Despite this conformational difference, a strong antigenic crossreactivity was observed between pep-a4 and the protein segment, as well as K156, a stabilized analogue of pep-a4 constrained into helix by seven helicogenic mutations, most of them involving hydrophobic residues.
For drastic mutations, most of them are relevant to glycine or proline.
Using DNA sequencing, we found almost exclusively rare mutations, most of which have been observed in other studies.
This structure contains 10 mutations, most of which belong to the DRC presently identified for the IDV-treated dataset.
PIK3CA mutations, most of which were in exons 9 and 20, were detected in 10 15% of patients with mCRC.
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Five of these patients presented more than one resistance mutation, most of which confer cross-resistance to more than one drug.
More than 60% (10/16) of the lung adenocarcinomas had a codon 12 mutation, most of which were G to T transversions.
Although our mutant strains were selected or chosen for specific phenotypes and therefore bias may occur for the causative mutation, most of the mutations arising throughout the genome will be random mutations unrelated to the observed phenotypes.
For example, the rho and rpoB trajectories differ in their associations with the cls gene; 23 of 30 clones with mutations in rho also contain a cls mutation, most of which interrupt cls function.
Fourteen different methods were used to detect BRAF mutations, most consisting of combinations of in-house techniques.
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