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The clinical significance of non-codon 600 mutations is largely unknown.
In populations with a small effective size, natural selection is less efficient, and hence, the fate of mutations is largely determined by random genetic drift.
The number of these mutations is largely underestimated because the impact on this finely orchestrated process (2– 4) is hardly predictable, particularly when considering nucleotide variations within exons (5, 6).
Variation in the rate of frameshift mutations is largely due to variation in the efficiency of mismatch repair across the genome, although the genomic feature responsible for this variation is unknown.
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We discovered that BAP1 is mutated in about 15% of clear-cell renal-cell carcinoma, and that BAP1 and PBRM1 mutations are largely mutually exclusive.
Nav1.2 mutations are largely associated with various epilepsy diseases, including BFIS3 (seizures, benign familial infantile 3), EIEE11 (epileptic encephalopathy, early infantile, 11), and DS (Fig. 3B and Table 3).
These mutations were largely responsible for the lack of significant Expect scores associated with the pfam protein domain analysis.
Although the mechanisms for these pleiotropic effects of IN mutations are largely unknown, there has been accumulating evidence for the involvement of retroviral INs in the reverse transcription [11], [13], [14], [18], [19].
In mammals, synonymous mutations are largely neutral, though they may sometimes experience weak selection [ 1].
In fact mitochondrial mutations are largely involved in various diseases, aging and cancer [ 12].
Mutations are largely missense, and are primarily to the head domain, potentially affecting the catalytic activity of MYH3.
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CEO of Professional Science Editing for Scientists @ prosciediting.com