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The domain-specific nature and unique phenotypic outcome of SSS mutations suggests a different pathogenetic mechanism from that of MFS.
Further investigation into location of mutations suggests a lack of direct interactions with YRS substrates or participation in enzyme dimerization.
Work in mice with targeted mutations suggests a role for several molecules in the development and function of TR cells.
The fact that S768I showed high frequencies in multiple mutations suggests a rationale for specific studies designed to explore the role of S768I in NSCLC oncogenesis.
A high prevalence and increasingly complex patterns of TDR-associated mutations suggests a generally high frequency of exposure in the treatment-naïve patients to diverse sources of viral strains.
Furthermore, the overexpression of wild-type p53 protein in human tumour specimens, as well as histologically benign lesions without p53 mutations, suggests a role for overexpression of p53 protein through overlapping mechanisms, idependent of actual p53 mutations (Barnes et al, 1992; Chozick et al, 1994b; Kurtkaya-Yapicier et al, 2002).
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In contrast, when six oncogenic mutations are required for cancer (C = 6), α50% ranges from 11 30 (Supplementary Table S1), in the lower range of commonly observed values of mutation rate increase due to mutator mutations, suggesting a predominance of mutator pathways, in that most mutator mutations would then correspond to α>α50%.
In contrast, when six oncogenic mutations are required for cancer (C = 6), α50% ranges from 11 30 (Supplementary Table S1), in the lower range of commonly observed values of mutation rate increase due to mutator mutations, suggesting a predominance of mutator pathways.
And most mutations suggest a propensity, not a guarantee, for a disease.
Leblond, C. S. et al. Genetic and functional analyses of SHANK2 mutations suggest a multiple hit model of autism spectrum disorders.
These modifications are possible by single point mutations, suggesting a potential yield of a more infectious virus.
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