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In the present study, we analyzed the mutations of four known drug resistance genes in both highland and lowland parasite populations of western Kenya.
To further examine the relative contribution of the two candidate miR-144-binding sites, mutations of four nucleotides in each seed-binding site (MUT1 and MUT2) and a mutation of two binding sites (MUT) were included, which abolish the putative miRNA-mRNA interactions.
Moreover, mutations of four putative calcium binding residues E698, E701, E730, and D734 differentially shifted the EC50 of channel activation to different calcium concentrations depending on the size and charge of the amino acid side chains, suggesting that these residues are likely involved in binding calcium.
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In that group, mutations of three genes are attributed to germination dormancy.
The iPLEX test included two plexes, which comprised seven mutations of the APC gene and 29 mutations of three of the mismatch repair genes.
Mutations of three genes all encoding ion-channels or membrane ionic pumps were discovered from 1996 to 2005.
Mutations of five amino acid residues in TEVpM2 slightly altered protein secondary structure conformed by circular dichroism assay.
Genetic interaction analysis, in which the combined mutations of two genes exhibit phenotypes significantly different from the single mutation of either one [1], is a powerful tool allowing biologists to investigate the genetic components of an organism [2].
To our interest, mutations of five conserved residues located within these two region had almost completely lost their ability to bind to the specific target DNA attB.
Examination of a public database indicated that homozygous mutations of five oncogenes were frequent (20%) in 833 cell lines of 12 tumor types.
Gain or loss-of-function mutations of one molecule have shown to affect alternative signaling pathways with a poorly understood mechanism.
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