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It remains to be characterized whether the presence of these relatively common mutations poses a risk for peripheral arterial disease (PAD).
However, the genomic heterogeneity of these resistance mutations poses a pharmacological challenge to develop selective KIT inhibitors that inhibit all possible mutations (Wardelmann et al, 2005).
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All of these mutations pose a serious challenge for the proteostasis network as they result not only in impaired function of the respective protein but also in ER stress, dysregulated proteasome, and altered autophagy function [25]-[27] [25]-[27]
The emergence of NAI-resistant variants of H7N9viruses with an NA R292K mutation poses a therapeutic challenge.
The variable expression of phenotypes, even among patients with the same GNAS mutation, poses a challenging problem and suggests a role of other genetic loci, epigenetic modifications, or environmental factors.
Particularly high background noise and artificial T > C substitutions at the position of the p.V654A mutation posed a problem and led to a higher detection limit.
Because of rapid increase in detection of the TR34/L98H mutation in many regions and its adverse effect on patient management, isolates harboring this mutation pose a serious public health threat.
But if only a small percentage of patients have each of the mutations, that poses a problem.
Our longitudinal study reflects the known allelic heterogeneity of RYR1 mutations which poses a challenge for effective variant identification strategies to the present day.
The distribution and frequency of these mutations poses serious questions about the sustainability of insecticide-based vector control programs.
Despite the recent success of gene-based complementation approaches for genetic recessive traits, the development of therapeutic strategies for gain-of-function mutations poses great challenges.
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