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This suggests that mutations rendering the CFTR non-functional are associated with a loss of airway bacterial (including pathogen) diversity and outgrowth of a small group of phylogenetically-related species as these patients age.
In summary, it was found that mutations rendering the SUB cSUBmut:EGFP construct nonfunctional also resulted in nonfunctional SUB gSUBmut:EGFP constructs, as corresponding SUB gSUBmut:EGFP sub-1 plants showed no rescue of the sub mutant phenotype (an example is given in Figure 6D).
The resulting mutation rate for changing allele 1 into allele 2 is U = r 19 10 − 8 = 8 19 10 − 8. Genes can also acquire null mutations, rendering the gene non-functional and therefore eliminating the organism.
When transiently expressed in tobacco pollen tubes, mutations rendering the more N-terminally located motif non-phosphorylatable (serines to alanines) resulted in longer pollen tubes, suggesting that phosphorylation negatively impacts growth.
Moreover, detailed analyses should include an assessment of the integrity of the meiosis-related genes identified, to rule out a recent accumulation of mutations rendering the genes non-functional (i.e., species-specific or even strain-specific loss of sex after isolation in culture).
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On the other hand, IDH1/2 missense mutations render the enzymes acquiring neomorphic activity that can convert α-KG to 2-HG (Dang et al., 2009).
These mutations render the ras proteins insensitive to GTP-induced hydrolysis of GTP to GDP and lock them in the activated state [ 2, 8, 9].
There is emerging evidence that at least some culture-adaptive mutations render the strains more sensitive to antibody neutralization (Dhillon et al., 2010; Grove et al., 2008).
However, the association with a β-like mutation (such as deletions, β39, and βIVSI-1 mutations) and even β+ mutations renders the phenotype of the heterozygous compound more severe.
Furthermore, the combination of both mutations renders the imbibed seeds of the atrad21.1 atradoubledouble mutant more hypersensitive to DNA dsb induction than the atrad21.1 and the atrad21.3 single mutants.
To understand the molecular basis for how these mutations render the kinase refractory to inhibition, we also solved the crystal structure of FGFR4K harboring the V550L gate-keeper mutation.
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