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Exact(5)
In the latter case, a silent mutation generating a novel SacII restriction site was identified in silico within codon 52 of phoQ using WatCut (http://watcut.uwaterloo.ca/) and the oligo sequences were modified accordingly [9] (Table 1, Fig. 3A).
We also identified a novel maternally inherited c.437C>T mutation, generating a proline to leucine missense mutation (p.P146L) in a conserved region of the H6PDH protein.
We identified four frameshifts within homopolymeric repeats, a nonsense mutation generating a truncation, and a missense mutation within a transmembrane region.
A mutation generating a stop codon was identified in the coding sequence for the kinetochore protein SPC105R in the IR8 mutant (Schittenhelm et al. 2009).
IFNL4 arises as a consequence of a frameshift mutation generating a new gene not normally expressed, and demonstrates only a 40.8% similarity to IFNL3. Figure 1A shows a sequence alignment of all IFNLs.
Similar(55)
This in-frame deletion mutation generates a local amino acid sequence at the fusion junction of what normally were distant polypeptide sequences in the intact epidermal growth factor receptor.
The antibody to N-terminal amino acids 740 1013 of mouse RBM44 was used in Figures 8 and 9 to confirm that our mutation generated a null mutation.
The lin-28 lf) lin-28 lfgenerates a precocious phenotype without the L2-specific symutationdivision; whereas, the lin-28(generatesion generates a retarded precociouswith further L2-like reiterations.
This mutation generates a premature stop, and is thought to generate a truncated non-functional protein.
This mutation generates a receptor in which the ability to transduce an apoptotic signal is blocked.
In the context of a delta-G polymorphism, the frameshift mutation generates a 'new' gene.
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