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We checked by direct sequencing that all differences between cpSSR size variants were due to variable numbers of mononucleotide repeats.
Some of the inaccurately imputed variants were due to poor clustering properties.
Thirdly, if the variants were due to inherited low-level heteroplasmy, we would not expect to see such variation across tissue types, since all tissue types derive from the fertilized egg.
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Recessive CPVT variants are due to mutations in the CASQ2 gene.
In contrast to the SPANX-A/D subfamily, none of the SPANX-N variants was due to gene conversion events.
It has been postulated that the success of these variants was due to either immune evasion or changes in receptor binding.
The enhanced sensitivity for detection of rare variants is due to the generation of non-interfering, individual signals for mutant and wild-type alleles.
It is possible the in vitro and in vivo properties observed in DinB Y79) variants are due to the inability of the new residue at position 79 to properly support F13 in carrying out high fidelity bypass.
Our finding that the evolutionary rates of R5 and X4 HIV-1 sub-populations are not significantly different support the hypothesis that amplification of X4 variants is due to factors other than an increased rate of evolution and may be linked to the availability of target cells.
Therefore, to determine whether the difference between the two VDR variants was due to disparities in VDR protein stability, the cells were exposed to the protein synthesis inhibitor cycloheximide (CHX, 10 µM) in the presence or absence of 1,25D3 for eight and sixteen hours.
That the BAK1 sequence variants are due to somatic events, which they dismiss as highly unlikely.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com