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The five key mutations could not be reversed first, because the receptor would be rendered useless.
By combining the current data with VH sequences obtained previously from the same cells, it was apparent that the repetitive silent mutations could not be explained solely by a genealogic tree.
Noise analysis of Orai1 Y80E and Y80K currents indicated that reductions in CDI for these mutations could not be accounted for by changes in unitary current or open probability.
Thus, although BLI kinetic analysis revealed a distinguishable kinetic trend between class 1 and class 2 mutations, the disease class associated with HIF-2α mutations could not be absolutely predicted solely by determining affinity for pVHL due to outliers like A530V.
Thus a prerequisite of unlinked loci within the whole group is needed and the recombination events between any two mutations could not be considered.
Therefore, the somatic status of these mutations could not be ascertained.
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These kinds of mutations couldn't be studied in mice because the corresponding mouse mutants would die in utero.
Finally, DNA# 54 was defined as 12Val-mutated by TheraScreen analysis, but this mutation could not be unequivocally confirmed in the PyroMark assay.
Using reverse genetics, combined mutations of Q253H and A284T could adapt vvIBDV to non-permissive CEF cells (rGx-F9VP2) but any single mutation could not.
In contrast to K833A plants, transgenic plants homozygous for the K519A mutation could not be obtained from the selfed progeny of T0 plants, although the growth conditions were similar to those of the K833A plants (Fig. 2a c, Table 1).
We also demonstrated that the RBD-Fc bearing R441A mutation could not bind to soluble and cell-associated angiotensin-converting enzyme 2 (ACE2), the functional receptor for SARS-CoV and failed to block S protein-mediated pseudovirus entry, indicating that this point mutation also disrupted the receptor-binding motif (RBM) in the RBD.
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