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Whatever you think of super-powered mutants, it would be impossible to deny their existence.
Since the VTC1 locus has also been characterized by cyt1 and emb101 mutants, it would seem that the mutant alleles might have some disadvantage in being propagated and a 'residual heterozygosity' might persist by some mechanism.
It would be nice to show integrated Q traces, analyze those, and compare them with what is seen for F. With the two other mutants, it would be interesting to see how these change.
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If Saibra was an X-Men mutant, it would mean she was Mystique, which means she would also be a villain.
As can also be deduced from Table 4, if working with DNA samples containing >70% tumor cells most of them mutant, it would be safe to analyze samples with wild-type DNA Cts<37.
If the phenotype is comparable to that of Clock mutant, it would suggest either the proposed role of USF1 in maintaining open chromatin structure is not essential or another USF family member can compensate for the loss of USF1.
By inserting the wt copy of this allele into dl mutant embryos, it would be possible to readily identify transgenic individuals at the larval stages of development.
We did not conduct immunohistochemistry for CP, but if increased CP is localized in the RGC layer of mutant animals, it would provide evidence that P4 Chrnb2−/− mice have higher rates of RGC death compared to WT animals.
Nevertheless, given that the NTE is necessary for the activity of some full-molecule ABC transporters, we suspect that even if a truncated polypeptide were generated in this mutant allele, it would not be functional [23], [24].
Therefore, for K-ras mutant patients, it would appear to be potentially harmful to treat them with EGFR-targeted therapy.
Although without careful evaluation of DNA content in Li 2 mutant fibers it would be too early to make conclusions.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com