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Moreover, the reduced hydroxylase activity due to the chy1, chy2 and lut5 mutations, reduces the rate of β-carotene processing into downstream xanthophylls, favoring its accumulation.
Contrary to our a priori expectation, the accumulation of spontaneous mutations reduces the variability in gene expression, as measured by the environmental (residual) component of variance (VE) of transcript abundance.
The presence of the K103N and Y181C mutations reduces the NNRTI binding affinity, leading to drug resistance.
The identification of causative mutations reduces the need for tag SNP (in linkage disequilibrium with causative mutations), promotes higher accuracy for genomic breeding values, which can persist over generations and permits a higher transferability across breeds [ 82].
One possible trivial explanation for this lethality is that the cluster of neutralizing mutations reduces the affinity of half hinges, which according to the ring model would accelerate dissociation of cohesin from chromatin.
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Computational modeling of the experimentally identified mutations showed that these mutations reduced the binding affinity through one of the three scenarios: through SCF destabilization, through elimination of favorable SCF/c-Kit intermolecular interactions, or through allosteric changes.
mop2 mutations reduce the abundance and activity of Pma1 protein on the plasma membrane without affecting the abundance of other prominent plasma membrane proteins.
On the other hand, mutations reduce the information content passed from generation to generation, thereby reducing the efficiency of selection.
In addition, some ALS-causing mutations reduce the affinity of the SOD protein for its zinc cofactor [41].
All these mutations reduce the ability of the receptor to respond to α-MSH (data not shown and [26], [32] [34].
In all cases, however, the substitution mutations reduced the frequency of termination-reinitiation events, albeit to a lesser extent with the 3' complementary extension mutant (Figure 3A).
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