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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).
This finding is significant since the same mutations render the construct catalytically dead, indicating that this activity is critical to the ability of rat CNP molecules to contribute to tRNA editing.
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.
The Fps1IVAA mutation prevents Hog1 binding to and regulation of Fps1, and Rgc27A cannot be displaced from Fps1 because it cannot be phosphorylated by Hog1; both mutations render the channel constitutively open and make cells arsenite sensitive (Lee et al., 2013 ).
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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).
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.
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.
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