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To assess the functional consequences of these four TRKB mutations, we determined their potential to suppress anoikis and to form tumors in nude mice.
To determine whether functional constraint may exist at the sites corresponding to the seven candidate mutations, we determined the orthologous major allele at each of the sites in chimpanzee, gorilla, orangutan, macaque, mouse and Fugu.
To test the functional impact of ECHS1 mutations, we determined 2-enoyl-CoA hydratase activity in the fibroblasts cell lysates from individuals F2, II.1 (#42031), F10, II:2 (#52236), F9, II:2 (#57277), and F5, II:3 (#73663).
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That is, after each mutation, we determined those alternative phenotypes that a mutated genotype could produce but that previous genotypes had not been able to produce, and appended these alternative phenotypes to a growing list of such phenotypes.
In those cases where we identified the genetic mutation, we determined the time to diagnosis.
In the TNBCs without a germline BRCA1 mutation, we determined the percentage of tumours with a BRCA1-like aCGH profile and with BRCA1 promoter methylation (Table 2b).
To determine whether DPY-21 influences dauer arrest generally as opposed to specifically in the context of eak-7 and akt-1 mutation, we determined the effect of reducing DPY-21 activity on dauer arrest in the background of other dauer-constitutive mutations using both dpy-21 RNAi and dpy-21 (null) genetic mutation.
Considering that 70% of human melanomas harbor BRAF activating mutations [3], we determined the phosphorylation status of LKB1Ser428 in different human melanoma cell lines harboring BRAFV600E activating mutations in serum free and complete medium conditions.
For each mutation rate, we determined the relationship between female preference and male gamete mutation load using the partial correlation between average female preference and average relative gamete mutation load for males across age classes, controlling for the effect of relative male somatic quality.
Because the error-prone polymerase UmuC plays a key role in accelerating the mutation frequency, we determined the influence of phototreatment on the development of spontaneous resistance to rifampicin.
Short read "next-generation" sequencing is relatively poor at reporting indels in simple sequence repeat regions (for further discussion see [ 13]), which might explain why the small indel mutation rates we determined are less than those previously determined by a different method for sexually propagated plants [ 14].
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com